Story 1: Want to live longer? Eat Less, Fast and Get Out More — Video

Posted on December 27, 2017. Filed under: Agriculture, Articles, Blogroll, Business, Diet, Disease, Documentary, Family, Food, government, liberty, Life, Links, media, Medicine, People, Philosophy, Photos, Rants, Raves, Raymond Thomas Pronk, Resources, Video, Welfare, Wisdom, Work | Tags: , , , , , , , , , , , , , , , , |

See the source imageSee the source image

See the source imageImage result for ketosisEat, Fast & Live Longer BBC Documentary

Eat Less – Live Longer

Eat Less, Live Longer

Keto and Intermittent Fasting for Beginners and…Procrastinators

Never Do Intermittent Fasting on a High Carbohydrate Diet

Keto and Intermittent Fasting: the Big Overview for Beginners

What Is Keto Adaptation?

How Long to Get Into Ketosis After Your Cheat Day

The Perfect Intermittent Fasting Ratio for the Most Weight Loss (Fat Burning)

5 Critical Ketosis Tips

The Biggest Mistake Doing Ketosis

7 Surprising Things That Can Kick You Out of Ketosis

9 Common Mistakes Everyone Makes Doing Keto (Ketogenic Diet)

How to do Intermittent Fasting for Serious Weight Loss

Ketosis – Healthy or Deadly?

Is Ketosis Safe Long Term?

How Long Does it Take to Get Into Ketosis?

How Much Fat Do I Eat: Ketogenic Diet?

The Ketogenic Diet & Dairy (Milk, Yogurt & Cheese)

The Best Greens for Salad is…

Finding a Good Salad Dressing is Not Easy

Make Your Own Balsamic Vinaigrette Dressing

Recipe for Homemade Italian Dressing

How to Make Homemade Mayonnaise

Best Nuts on a Ketogenic Diet: SURPRISING!

What is “Too Much” Fat on Keto (ketogenic diet)?

Protein to Fat Ratio on a Keto and Intermittent Fasting Plan

 

Anti Aging Diet: On Calorie Restriction for over 20 years

Roy Walford interview by M. MacRae, part 1

Roy Walford interview by M. MacRae, part 2

Why bodybuilding at age 93 is a great idea: Charles Eugster at TEDxZurich

How to die young at a very old age | Nir Barzilai | TEDxGramercy

Fasting: A Path To Mental And Physical Transcendence | Phil Sanderson | TEDxBeaconStreet

Why fasting bolsters brain power: Mark Mattson at TEDxJohnsHopkinsUniversity

Run for your life! At a comfortable pace, and not too far: James O’Keefe at TEDxUMKC

 

 

Leaving the house linked to longevity in older adults

By Carolyn Crist

,

Reuters

By Carolyn Crist

(Reuters Health) – For older people, getting out of the house regularly may contribute to a longer life – and the effect is independent of medical problems or mobility issues, according to new research from Israel.

For study participants in their 70s, 80s and 90s, the frequency with which they left the house predicted how likely they were to make it to the next age milestone, researchers report in Journal of the American Geriatrics Society.

“The simple act of getting out of the house every day propels people into engagement with the world,” said lead author Dr. Jeremy Jacobs of Hadassah-Hebrew University Medical Center in Jerusalem in a phone interview.

“We saw similar benefits that you’d expect from treating blood pressure or cholesterol with medicine,” Jacobs said. “Social factors are important in the process of aging.”

Jacobs and colleagues analyzed data on 3,375 adults at ages 70, 78, 85 and 90 who were participating in the Jerusalem Longitudinal Study.

Based on their responses to questions about how often they left the house, participants were grouped into three categories: frequently (six or seven days per week), often (two to five times per week) or rarely (once a week or less).

People who left the house frequently at any of the ages examined were significantly more likely to live to the next age group. For example, among people who left the house frequently, often or rarely at age 78, 71 percent, 67 percent and 43 percent, respectively, survived to age 85. Among people who left the house frequently, often or rarely at age 90, 64 percent, 56 percent and 38 percent, respectively, made it to 95.

At all ages, people who left home less frequently tended to be male, less educated and to have higher rates of loneliness, financial difficulties, poor health, fatigue, poor sleep, less physical activity, bladder and bowel problems, history of falling in the last year, fear of falling, visual and hearing impairments, chronic pain and frailty.

The link between leaving the house and longevity, however, remained after the researchers accounted for medical or mobility issues such as chronic pain, vision or hearing impairment, diabetes, hypertension, heart disease and kidney disease.

“We included people who had mobility difficulties, so this isn’t just about people moving their legs up and down,” Jacobs said. “That’s quite exciting. There’s something about interacting with the world outside that helps.”

The study did not examine the effect on participants of leaving the house, such as their sense of wellbeing or purpose. It also didn’t look at environmental factors that might foster or prevent going out, the authors note.

Future studies will look at the oldest cohort (age 95) as they reach 98 to 100 in coming years, Jacobs said. He and his colleagues are also interested in the role that optimism, social engagement and environmental aspects such as community sidewalks play in longer life.

“Studies show that if you create walkways that are friendly for walking, people start walking,” he said. “In neighborhoods with older adults, walkways with benches could encourage them to get out of the house and be social.”

Researchers are interested in finding ways to encourage adults to leave their home more and to develop systems that help them do that, said Dawn Mackey of Simon Fraser University in Vancouver, Canada, who wasn’t involved in the study.

“It may be helpful for older adults and their caregivers to make plans to go out of the house more often,” she told Reuters Health by email. “And try to build up to going out of the house every day.”

They could plan these outings with these questions: When will it work best for me to leave the house? Where do I want to go? Is there someone to go out with or to meet when I am out? What are my options if the weather is bad or if I’m not feeling well one day?

“The wellbeing of our older adults is of paramount importance for public health and economic viability,” she said. “Going out of the house is an important way to maintain mobility and social engagement and ward off loneliness.”

SOURCE: http://bit.ly/2DVrdwP Journal of the American Geriatrics Society, online November 22, 2017.

https://www.yahoo.com/news/leaving-house-linked-longevity-older-adults-182911297.html

Roy Walford

From Wikipedia, the free encyclopedia
Roy Walford
Born June 29, 1924
San Diego
Died April 27, 2004 (aged 79)
Santa Monica, California, US
Residence Venice, California, US
Known for life extension

Roy Lee Walford, M. D. (June 29, 1924 – April 27, 2004) was a pioneer in the field of caloric restriction. He died at age 79 of respiratory failure as a complication of amyotrophic lateral sclerosis (commonly known as Lou Gehrig’s or motor neurone disease). He was a leading advocate of calorie restriction as a method of life extension and health improvement.

Career highlights

Walford is credited with significantly furthering aging research by his discovery that laboratory mice, when fed a diet that restricted their caloric intake by 50% yet maintaining nutritional requirements, almost doubled their expected life span.

He received his medical degree from the University of Chicago in 1948. He completed his internship at Gorgas HospitalPanama, and served his residency at the V.A. Medical Center in Los Angeles. He then served two years in the US Air Force during the Korean War.

Walford joined the faculty at the University of California at Los Angeles (UCLA) in 1954. He became a Professor of Pathology at the UCLA School of Medicine in 1966. He became Professor of Pathology and Laboratory Medicine, Emeritus, for UCLA, when he left to join the crew of Biosphere 2 in 1991.

While at UCLA, Walford served in the following roles:

  • Director of the Blood Bank and of the Hematology Division of the Clinical Laboratories (1959–1980)
  • Director of the School of Medical Technology (1962–1972)
  • Chairman of the Vivarium Committee (1965–1968)

In addition to his service at UCLA, he was an expert advisor in immunology for the World Health Organization from 1969 to 1984, was a senatorial delegate to the White House Conference on Aging in 1981, and a member of the National Institute on Aging.

His honors and awards include:[1]

  • Levine Award of the American Society of Clinical Pathology
  • Research Award of the American Aging Association
  • Kleemeier Award from the Gerontological Society of America
  • Henderson Award from the American Geriatrics Society
  • 1998 Longevity Prize of the Fondation IPSEN[2]
  • The Senator Alan Cranston Award
  • Infinity Award of the American Academy of Anti-Aging Medicine
  • Asteroid #4629 was named after him by its discoverer (E. Helene) in 1986

Walford and his work were featured in print in dozens of articles in popular publications such as OmniDiscover, and Scientific American. During his life he also made dozens of featured appearances on various television shows.

Roulette winnings

In 1947, while on vacation during medical school, Walford and Albert Hibbs, a mathematics graduate student, used statistical analysis of biased roulette wheels to “break the bank” in Reno. They tracked the results of the spins, determined which wheels were biased, and then bet heavily on the ones which were unbalanced. The casinos eventually realized that Walford and his friend knew what they were doing and threw them out. A Life Magazine photographer captured the pair drinking milk and counting their chips in a photograph published in the December 8, 1947 issue.[3] Their methods were also mentioned in the roulette book The Eudaemonic Pie by Thomas Bass. Different sources have the pair winning anywhere from $6,500[3] to $42,000.[4] The high end is more likely, as Walford was reputed to have paid for part of his medical school education and a house from his winnings. The pair also bought a yacht and sailed the Caribbean for over a year.

Gerontix

In 1981, Walford began a commercial collaboration with fellow researchers Richard Weindruch and Kathleen Yankee Hall, and her husband William Hall, a wealthy businessman. In her tribute after his death, Kathleen Hall wrote of Walford, “we both threw in a few thousand dollars and started a small business together.”[5] Incorporated in California as Gerontix, the company was to sell supplements intended to improve health and increase life span. The first Gerontix product was butylated hydroxytoluene (BHT), with lysine and zinc, which was sold in capsules and marketed as a treatment for herpes. Motivated by the success of the bestselling book Life Extension: A Practical Scientific Approach, by Durk Pearson and Sandy Shaw, the group intended to sell a package of products, called MaxiLife, which would capitalize on the release of Walford’s book, Maximum Life Span. It was expected that Walford, a highly publicized researcher, would experience the same success as Pearson and Shaw. Before Walford’s book was published and Gerontix started to manufacture its coordinated products, the manufacturer Twin Labs began to sell a single multi-ingredient supplement called MaxiLIFE. Despite the potential for trademark conflict, the Gerontix group elected to proceed with plans to use the name. Twin Labs brought suit against Gerontix for trademark infringement, which it won in 1984. Before the resolution of the lawsuit, the Gerontix MaxiLife[6] products were brought to market and sold poorly, partly because of the lackluster sales of Walford’s book. Lack of success in federal court and in health food stores led to the demise of Gerontix.

In Appendix B of Walford’s Maximum Life Span he noted, “Additional additives, such as antioxidants and some of the other materials I’ve listed in Chapters 7 and 8, can be obtained from Gerontix Biological Research Products…,”[7] but he did not disclose that he would profit from the sale of Gerontix products. The company’s MaxiLife product brochure, which refers to Walford and his research, also makes no mention of his connection to Gerontix.[6]

Biosphere 2

Walford was one of the eight “crew members” who were sealed inside Biosphere 2 where they lived from September 26, 1991 to September 26, 1993. Walford served as the crew’s physician. During his stay in Biosphere 2, the crew found that they could not grow as much food as anticipated, so Walford convinced the crew to follow his calorie restriction diet.[8] It is claimed that this action “produced dramatic weight loss and improved health.”[9] Despite this, in November of the first year the crew decided to open a cache of emergency food supplies grown outside of the bubble to supplement their meager diets.[10]

Caloric restriction and ALS

Walford’s death from amyotrophic lateral sclerosis (ALS) has provoked consideration about whether his practice of caloric restriction (CR) may have contributed to, or accelerated, his development of the disease. Research on a transgenic mouse model of ALS demonstrates that CR may hasten the onset of death in ALS. Hamadeh et al. therefore concluded, “These results suggest that CR diet is not a protective strategy for patients with amyotrophic lateral sclerosis (ALS) and hence is contraindicated.”[11] Hamadeh et al. also note two human studies[12] that show “low energy intake correlates with death in people with ALS.” However, in the first study, Slowie, Paige, and Antel state, “The reduction in energy intake by ALS patients did not correlate with the proximity of death but rather was a consistent aspect of the illness.” They conclude, “ALS patients have a chronically deficient intake of energy and recommended augmentation of energy intake.”[12]

Previously, Pedersen and Mattson found that in the ALS mouse model, CR “accelerates the clinical course” of the disease and had no benefits.[13] Suggesting that a calorically dense diet may slow ALS, a ketogenic diet in the ALS mouse model has been shown to slow the progress of disease.[14] More recently, Mattson et al. opine that the death by ALS of Roy Walford, a pioneer in CR research and its antiaging effects, may have been a result of his own practice of CR.[15] However, as Mattson et al. acknowledge, Walford’s single case is insufficient to establish the proposed a cause-effect relation.

Walford himself speculated that his disease may have been caused by the combination of chronic hypoxia and exposure to carbon monoxide and nitrous oxide in Biosphere 2.[16]

Life’s end

According to Walford’s friend and colleague, Kathleen Hall, his diagnosis of ALS came as a result of her urging him to see a physician when she noticed “the strangeness in Roy’s gait.”[5] She says that before his death Walford “continued writing, taking courses on film production. He had me all over New York and in Dallas for just the right production shots.” Meanwhile, Hall remembers that “Roy and I together with his daughter, Lisa, and his friends exhausted all the literature, looking for a cure, a solution. I found myself scouting the alleys of Chinatown in New York searching out a particular mushroom, looking for the best grass to help him through the pain.”[5] Even before developing ALS, Walford was no stranger to “grass.” In his book Eternity Soup: Inside the Quest to End AgingGreg Critser says that Walford’s “consumption of marijuana was legendary.”[17]

Published works

Walford authored several books, and set out his dietary beliefs in the bestseller Beyond the 120-Year Diet. In addition, he published at least 340 scientific papers, mainly focused on the biology of aging.

Walford authored or co-authored the following books:[18]

  • R. L. Walford (1960). Leukocyte Antigens and Antibodies. New York: Grune and Stratton, Inc.
  • R. L. Walford (1969). The Isoantigenic Systems of Human Leukocytes: Medical and Biological SignificanceSeries Haematologica 22. Copenhagen: Munksgaard. pp. 1–96.
  • R. L. Walford (1969). The Immunological Theory of Aging. Copenhagen: Munksgaard.
  • R. L. Walford (1983). Maximum Life Span. New York: W.W. Norton & Co. ISBN 0-380-65524-1.
  • R. L. Walford (1986). The 120-Year Diet. New York: Simon and Schuster. ISBN 0-671-64904-3.
  • R. H. Weindruch and R. L. Walford (1988). The Retardation of Aging and Disease by Dietary Restriction. New York: Charles C. Thomas.
  • R. L. Walford and Lisa J. Walford (1994). The Anti-Aging Plan. New York: Four Walls Eight Windows. ISBN 1-56924-383-2.
  • R. L. Walford (2000). Beyond The 120-Year Diet. New York: Four Walls Eight Windows. ISBN 1-56858-157-2.

References

https://en.wikipedia.org/wiki/Roy_Walford

Ketogenic diet

From Wikipedia, the free encyclopedia
Ketogenic diet
A test strip is compared with a colour chart that indicates the degree of ketonuria.

MeSH D055423

The ketogenic diet is a high-fat, adequate-proteinlow-carbohydrate diet that in medicine is used primarily to treat difficult-to-control (refractory) epilepsy in children. The diet forces the body to burn fats rather than carbohydrates. Normally, the carbohydrates contained in food are converted into glucose, which is then transported around the body and is particularly important in fueling brain-function. However, if there is very little carbohydrate in the diet, the liver converts fat into fatty acids and ketone bodies. The ketone bodies pass into the brain and replace glucose as an energy source. An elevated level of ketone bodies in the blood, a state known as ketosis, leads to a reduction in the frequency of epileptic seizures.[1] Almost half of children, and young people, with epilepsy who have tried some form of this diet saw the number of seizures drop by at least half, and the effect persists even after discontinuing the diet.[2] There is some evidence that adults with epilepsy may benefit from the diet, and that a less strict regimen, such as a modified Atkins diet, is similarly effective.[1] The most common adverse effect is constipation, affecting about 30% of patients—this was due to fluid restriction, which was once a feature of the diet, but this led to increased risk of kidney stones, and is no longer considered beneficial.[2][3]

The original therapeutic diet for paediatric epilepsy provides just enough protein for body growth and repair, and sufficient calories[Note 1] to maintain the correct weight for age and height. The classic therapeutic ketogenic diet was developed for treatment of paediatric epilepsy in the 1920s and was widely used into the next decade, but its popularity waned with the introduction of effective anticonvulsant medications. This classic ketogenic diet contains a 4:1 ratio by weight of fat to combined protein and carbohydrate. This is achieved by excluding high-carbohydrate foods such as starchy fruits and vegetables, bread, pasta, grains and sugar, while increasing the consumption of foods high in fat such as nuts, cream, and butter.[1] Most dietary fat is made of molecules called long-chain triglycerides (LCTs). However, medium-chain triglycerides (MCTs)—made from fatty acids with shorter carbon chains than LCTs—are more ketogenic. A variant of the classic diet known as the MCT ketogenic diet uses a form of coconut oil, which is rich in MCTs, to provide around half the calories. As less overall fat is needed in this variant of the diet, a greater proportion of carbohydrate and protein can be consumed, allowing a greater variety of food choices.[4][5]

In the mid-1990s, Hollywood producer Jim Abrahams, whose son’s severe epilepsy was effectively controlled by the diet, created the Charlie Foundation to promote it. Publicity included an appearance on NBC’s Dateline programme and …First Do No Harm (1997), a made-for-television film starring Meryl Streep. The foundation sponsored a multicentre research study, the results of which—announced in 1996—marked the beginning of renewed scientific interest in the diet.[1]

Clinical trials and studies in animal models (including C. elegans[6]) suggest that ketogenic diets provide neuroprotective and disease-modifying benefits for a number of adult neurodegenerative disorders.[7][8] As of 2012, there is limited clinical trial data in these areas, and, outside of paediatric epilepsy, use of the ketogenic diet remains at the research stage.[3][9][10]

Epilepsy

Epilepsy is one of the most common neurological disorders after stroke,[11] and affects at least 50 million people worldwide.[12] It is diagnosed in a person having recurrent unprovoked seizures. These occur when cortical neurons fire excessively, hypersynchronously, or both, leading to temporary disruption of normal brain function. This might affect, for example, the muscles, the senses, consciousness, or a combination. A seizure can be focal (confined to one part of the brain) or generalised (spread widely throughout the brain and leading to a loss of consciousness). Epilepsy may occur for a variety of reasons; some forms have been classified into epileptic syndromes, most of which begin in childhood. Epilepsy is considered refractory (not yielding to treatment) when two or three anticonvulsant drugs have failed to control it. About 60% of patients will achieve control of their epilepsy with the first drug they use, whereas about 30% do not achieve control with drugs. When drugs fail, other options include epilepsy surgeryvagus nerve stimulation and the ketogenic diet.[11]

History

The ketogenic diet is a mainstream therapy that does not use pharmaceutical drugs, which was developed to reproduce the success and remove the limitations of the non-mainstream use of fasting to treat epilepsy.[Note 2] Although popular in the 1920s and 30s, it was largely abandoned in favour of new anticonvulsant drugs.[1] Most individuals with epilepsy can successfully control their seizures with medication. However, 20–30% fail to achieve such control despite trying a number of different drugs.[9] For this group, and for children in particular, the diet has once again found a role in epilepsy management.[1][13]

Fasting

Scan of newspaper column. See image description page for full text.

A news report of Dr Hugh Conklin’s “water diet” treatment from 1922

Physicians of ancient Greece treated diseases, including epilepsy, by altering their patients’ diet. An early treatise in the Hippocratic CorpusOn the Sacred Disease, covers the disease; it dates from c. 400 BC. Its author argued against the prevailing view that epilepsy was supernatural in origin and cure, and proposed that dietary therapy had a rational and physical basis.[Note 3] In the same collection, the author of Epidemics describes the case of a man whose epilepsy is cured as quickly as it had appeared, through complete abstinence of food and drink.[Note 4] The royal physician Erasistratusdeclared, “One inclining to epilepsy should be made to fast without mercy and be put on short rations.”[Note 5] Galen believed an “attenuating diet”[Note 6]might afford a cure in mild cases and be helpful in others.[14]

The first modern study of fasting as a treatment for epilepsy was in France in 1911.[15] Twenty epilepsy patients of all ages were “detoxified” by consuming a low-calorie vegetarian diet, combined with periods of fasting and purging. Two benefited enormously, but most failed to maintain compliance with the imposed restrictions. The diet improved the patients’ mental capabilities, in contrast to their medication, potassium bromide, which dulled the mind.[16]

Around this time, Bernarr Macfadden, an American exponent of physical culture, popularised the use of fasting to restore health. His disciple, the osteopathic physician Hugh Conklin, of Battle Creek, Michigan, began to treat his epilepsy patients by recommending fasting. Conklin conjectured that epileptic seizures were caused when a toxin, secreted from the Peyer’s patches in the intestines, was discharged into the bloodstream. He recommended a fast lasting 18 to 25 days to allow this toxin to dissipate. Conklin probably treated hundreds of epilepsy patients with his “water diet” and boasted of a 90% cure rate in children, falling to 50% in adults. Later analysis of Conklin’s case records showed 20% of his patients achieved freedom from seizures and 50% had some improvement.[13]

Conklin’s fasting therapy was adopted by neurologists in mainstream practice. In 1916, a Dr McMurray wrote to the New York Medical Journal claiming to have successfully treated epilepsy patients with a fast, followed by a starch- and sugar-free diet, since 1912. In 1921, prominent endocrinologist H. Rawle Geyelin reported his experiences to the American Medical Associationconvention. He had seen Conklin’s success first-hand and had attempted to reproduce the results in 36 of his own patients. He achieved similar results despite only having studied the patients for a short time. Further studies in the 1920s indicated that seizures generally returned after the fast. Charles Howland, the parent of one of Conklin’s successful patients and a wealthy New York corporate lawyer, gave his brother John a gift of $5,000 to study “the ketosis of starvation”. As professor of paediatrics at Johns Hopkins Hospital, John Howland used the money to fund research undertaken by neurologist Stanley Cobb and his assistant William G. Lennox.[13]

Diet

In 1921, Rollin Woodyatt reviewed the research on diet and diabetes. He reported that three water-soluble compounds, β-hydroxybutyrateacetoacetate and acetone (known collectively as ketone bodies), were produced by the liver in otherwise healthy people when they were starved or if they consumed a very low-carbohydrate, high-fat diet. Russel Wilder, at the Mayo Clinic, built on this research and coined the term ketogenic diet to describe a diet that produced a high level of ketone bodies in the blood (ketonemia) through an excess of fat and lack of carbohydrate. Wilder hoped to obtain the benefits of fasting in a dietary therapy that could be maintained indefinitely. His trial on a few epilepsy patients in 1921 was the first use of the ketogenic diet as a treatment for epilepsy.[13]

Wilder’s colleague, paediatrician Mynie Peterman, later formulated the classic diet, with a ratio of one gram of protein per kilogram of body weight in children, 10–15 g of carbohydrate per day, and the remainder of calories from fat. Peterman’s work in the 1920s established the techniques for induction and maintenance of the diet. Peterman documented positive effects (improved alertness, behaviour and sleep) and adverse effects (nausea and vomiting due to excess ketosis). The diet proved to be very successful in children: Peterman reported in 1925 that 95% of 37 young patients had improved seizure control on the diet and 60% became seizure-free. By 1930, the diet had also been studied in 100 teenagers and adults. Clifford Barborka, also from the Mayo Clinic, reported that 56% of those older patients improved on the diet and 12% became seizure-free. Although the adult results are similar to modern studies of children, they did not compare as well to contemporary studies. Barborka concluded that adults were least likely to benefit from the diet, and the use of the ketogenic diet in adults was not studied again until 1999.[13][17]

Anticonvulsants and decline

During the 1920s and 1930s, when the only anticonvulsant drugs were the sedative bromides (discovered 1857) and phenobarbital (1912), the ketogenic diet was widely used and studied. This changed in 1938 when H. Houston Merritt and Tracy Putnam discovered phenytoin (Dilantin), and the focus of research shifted to discovering new drugs. With the introduction of sodium valproate in the 1970s, drugs were available to neurologists that were effective across a broad range of epileptic syndromes and seizure types. The use of the ketogenic diet, by this time restricted to difficult cases such as Lennox–Gastaut syndrome, declined further.[13]

MCT diet

A glass bottle of 250 ml of Liquigen, a white opaque liquid

Medium-chain triglyceride (MCT) oil emulsion

In the 1960s, it was discovered that medium-chain triglycerides (MCTs) produce more ketone bodies per unit of energy than normal dietary fats (which are mostly long-chain triglycerides).[18] MCTs are more efficiently absorbed and are rapidly transported to the liver via the hepatic portal system rather than the lymphatic system.[19] The severe carbohydrate restrictions of the classic ketogenic diet made it difficult for parents to produce palatable meals that their children would tolerate. In 1971, Peter Huttenlocher devised a ketogenic diet where about 60% of the calories came from the MCT oil, and this allowed more protein and up to three times as much carbohydrate as the classic ketogenic diet. The oil was mixed with at least twice its volume of skimmed milk, chilled, and sipped during the meal or incorporated into food. He tested it on twelve children and adolescents with intractable seizures. Most children improved in both seizure control and alertness, results that were similar to the classic ketogenic diet. Gastrointestinal upset was a problem, which led one patient to abandon the diet, but meals were easier to prepare and better accepted by the children.[18] The MCT diet replaced the classic ketogenic diet in many hospitals, though some devised diets that were a combination of the two.[13]

Revival

The ketogenic diet achieved national media exposure in the US in October 1994, when NBC’s Dateline television programme reported the case of Charlie Abrahams, son of Hollywood producer Jim Abrahams. The two-year-old suffered from epilepsy that had remained uncontrolled by mainstream and alternative therapies. Abrahams discovered a reference to the ketogenic diet in an epilepsy guide for parents and brought Charlie to John Freemanat Johns Hopkins Hospital, which had continued to offer the therapy. Under the diet, Charlie’s epilepsy was rapidly controlled and his developmental progress resumed. This inspired Abrahams to create the Charlie Foundation to promote the diet and fund research.[13] A multicentre prospective study began in 1994, the results were presented to the American Epilepsy Society in 1996 and were published[20] in 1998. There followed an explosion of scientific interest in the diet. In 1997, Abrahams produced a TV movie, …First Do No Harm, starring Meryl Streep, in which a young boy’s intractable epilepsy is successfully treated by the ketogenic diet.[1]

By 2007, the ketogenic diet was available from around 75 centres in 45 countries, and less restrictive variants, such as the modified Atkins diet, were in use, particularly among older children and adults. The ketogenic diet was also under investigation for the treatment of a wide variety of disorders other than epilepsy.[1]

Efficacy

The ketogenic diet reduces seizure frequency by more than 50% in half of the patients who try it and by more than 90% in a third of patients.[3] Three-quarters of children who respond do so within two weeks, though experts recommend a trial of at least three months before assuming it has been ineffective.[9] Children with refractory epilepsy are more likely to benefit from the ketogenic diet than from trying another anticonvulsant drug.[1] There is some evidence that adolescents and adults may also benefit from the diet.[9]

Trial design

Early studies reported high success rates: in one study in 1925, 60% of patients became seizure-free, and another 35% of patients had a 50% reduction in seizure frequency. These studies generally examined a cohort of patients recently treated by the physician (what is known as a retrospective study) and selected patients who had successfully maintained the dietary restrictions. However, these studies are difficult to compare to modern trials. One reason is that these older trials suffered from selection bias, as they excluded patients who were unable to start or maintain the diet and thereby selected from patients who would generate better results. In an attempt to control for this bias, modern study design prefers a prospective cohort (the patients in the study are chosen before therapy begins) in which the results are presented for all patients regardless of whether they started or completed the treatment (known as intent-to-treat analysis).[21]

Another difference between older and newer studies is that the type of patients treated with the ketogenic diet has changed over time. When first developed and used, the ketogenic diet was not a treatment of last resort; in contrast, the children in modern studies have already tried and failed a number of anticonvulsant drugs, so may be assumed to have more difficult-to-treat epilepsy. Early and modern studies also differ because the treatment protocol has changed. In older protocols, the diet was initiated with a prolonged fast, designed to lose 5–10% body weight, and heavily restricted the calorie intake. Concerns over child health and growth led to a relaxation of the diet’s restrictions.[21] Fluid restriction was once a feature of the diet, but this led to increased risk of constipation and kidney stones, and is no longer considered beneficial.[3]

Outcomes

A study with an intent-to-treat prospective design was published in 1998 by a team from the Johns Hopkins Hospital[22] and followed-up by a report published in 2001.[23] As with most studies of the ketogenic diet, there was no control group (patients who did not receive the treatment). The study enrolled 150 children. After three months, 83% of them were still on the diet, 26% had experienced a good reduction in seizures, 31% had had an excellent reduction and 3% were seizure-free.[Note 7] At twelve months, 55% were still on the diet, 23% had a good response, 20% had an excellent response and 7% were seizure-free. Those who had discontinued the diet by this stage did so because it was ineffective, too restrictive or due to illness, and most of those who remained were benefiting from it. The percentage of those still on the diet at two, three and four years was 39%, 20% and 12% respectively. During this period the most common reason for discontinuing the diet was because the children had become seizure-free or significantly better. At four years, 16% of the original 150 children had a good reduction in seizure frequency, 14% had an excellent reduction and 13% were seizure-free, though these figures include many who were no longer on the diet. Those remaining on the diet after this duration were typically not seizure-free but had had an excellent response.[23][24]

It is possible to combine the results of several small studies to produce evidence that is stronger than that available from each study alone—a statistical method known as meta-analysis. One of four such analyses, conducted in 2006, looked at 19 studies on a total of 1,084 patients.[25] It concluded that half the patients achieved a 50% reduction in seizures and a third achieved a 90% reduction.[3]

A systematic review in 2012 found and analysed four randomized controlled trials of ketogenic diet in children and young people with epilepsy, as well as six prospective and five retrospective studies.[2] The trials were done among children and young people for whom drugs failed to control their seizures, and only one of the trials compared a group assigned to ketogenic diet with a group not assigned to one.[19] The other trials compared types of diets or ways of introducing them to make them more tolerable.[2] Nearly 40% of the children and young people had half or fewer seizures with the diet compared with the group not assigned to the diet. Only about 10% were still on the diet after a few years.[2] Adverse effects such as hunger and loss of energy in that trial were common, with about 30% experiencing constipation.[19]

Indications and contra-indications

Anticonvulsants

Experts on the ketogenic diet recommend it be strongly considered for children with uncontrolled epilepsy who have tried and failed two or three anticonvulsant drugs;[9] most children who start the ketogenic diet have failed at least three times this number.[26]

The ketogenic diet is indicated as an adjunctive (additional) treatment in children with drug-resistant epilepsy.[27][28] It is approved by national clinical guidelines in Scotland,[28] England and Wales[27] and reimbursed by nearly all US insurance companies.[29] Children with a focal lesion (a single point of brain abnormality causing the epilepsy) who would make suitable candidates for surgery are more likely to become seizure-free with surgery than with the ketogenic diet.[9][30] In the UK, the National Institute for Health and Clinical Excellence advises that the diet should not be recommended for adults with epilepsy.[27] About a third of epilepsy centres that offer the ketogenic diet also offer a dietary therapy to adults. Some clinicians consider the two less restrictive dietary variants—the low glycaemic index treatment and the modified Atkins diet—to be more appropriate for adolescents and adults.[9] A liquid form of the ketogenic diet is particularly easy to prepare for, and well tolerated by, infants on formula and children who are tube-fed.[5][31]

Advocates for the diet recommend that it be seriously considered after two medications have failed, as the chance of other drugs succeeding is only 10%.[9][32][33] The diet can be considered earlier for some epilepsy and genetic syndromes where it has shown particular usefulness. These include Dravet syndromeinfantile spasmsmyoclonic-astatic epilepsy and tuberous sclerosis complex.[9][34]

A survey in 2005 of 88 paediatric neurologists in the US found that 36% regularly prescribed the diet after three or more drugs had failed; 24% occasionally prescribed the diet as a last resort; 24% had only prescribed the diet in a few rare cases; and 16% had never prescribed the diet. There are several possible explanations for this gap between evidence and clinical practice.[35] One major factor may be the lack of adequately trained dietitians, who are needed to administer a ketogenic diet programme.[32]

Because the ketogenic diet alters the body’s metabolism, it is a first-line therapy in children with certain congenital metabolic diseases such as pyruvate dehydrogenase (E1) deficiency and glucose transporter 1 deficiency syndrome, which prevent the body from using carbohydrates as fuel, leading to a dependency on ketone bodies. The ketogenic diet is beneficial in treating the seizures and some other symptoms in these diseases and is an absolute indication.[36] On the other hand, it is absolutely contraindicated in the treatment of other diseases such as pyruvate carboxylase deficiencyporphyriaand other rare genetic disorders of fat metabolism.[9] A person with a disorder of fatty acid oxidation is unable to metabolise fatty acids, which replace carbohydrates as the major energy source on the diet. On the ketogenic diet, their body would consume its own protein stores for fuel, leading to ketoacidosis, and eventually coma and death.[37]

Interactions

The ketogenic diet is usually initiated in combination with the patient’s existing anticonvulsant regimen, though patients may be weaned off anticonvulsants if the diet is successful. There is some evidence of synergistic benefits when the diet is combined with the vagus nerve stimulator or with the drug zonisamide, and that the diet may be less successful in children receiving phenobarbital.[3]

Adverse effects

The ketogenic diet is not a benign, holistic or natural treatment for epilepsy; as with any serious medical therapy, there may be complications.[29] These are generally less severe and less frequent than with anticonvulsant medication or surgery.[29] Common but easily treatable short-term side effects include constipation, low-grade acidosis and hypoglycaemia if there is an initial fast. Raised levels of lipids in the blood affect up to 60% of children[38] and cholesterol levels may increase by around 30%.[29] This can be treated by changes to the fat content of the diet, such as from saturated fats towards polyunsaturated fats, and, if persistent, by lowering the ketogenic ratio.[38] Supplements are necessary to counter the dietary deficiency of many micronutrients.[3]

Long-term use of the ketogenic diet in children increases the risk of slowed or stunted growth, bone fractures and kidney stones.[3] The diet reduces levels of insulin-like growth factor 1, which is important for childhood growth. Like many anticonvulsant drugs, the ketogenic diet has an adverse effect on bone health. Many factors may be involved such as acidosis and suppressed growth hormone.[38] About 1 in 20 children on the ketogenic diet will develop kidney stones (compared with one in several thousand for the general population). A class of anticonvulsants known as carbonic anhydrase inhibitors (topiramatezonisamide) are known to increase the risk of kidney stones, but the combination of these anticonvulsants and the ketogenic diet does not appear to elevate the risk above that of the diet alone.[39] The stones are treatable and do not justify discontinuation of the diet.[39] Johns Hopkins Hospital now gives oral potassium citrate supplements to all ketogenic diet patients, resulting in a sevenfold decrease in the incidence of kidney stones.[40] However, this empiric usage has not been tested in a prospective controlled trial.[9] Kidney stone formation (nephrolithiasis) is associated with the diet for four reasons:[39]

  • Excess calcium in the urine (hypercalciuria) occurs due to increased bone demineralisation with acidosis. Bones are mainly composed of calcium phosphate. The phosphate reacts with the acid, and the calcium is excreted by the kidneys.[39]
  • Hypocitraturia: the urine has an abnormally low concentration of citrate, which normally helps to dissolve free calcium.[39]
  • The urine has a low pH, which stops uric acid from dissolving, leading to crystals that act as a nidus for calcium stone formation.[39]
  • Many institutions traditionally restricted the water intake of patients on the diet to 80% of normal daily needs;[39] this practice is no longer encouraged.[3]

In adolescent and adults, common side effects reported include weight loss, constipation, dyslipidemia and, in women, dysmenorrhea.[41]

Implementation

The ketogenic diet is a medical nutrition therapy that involves participants from various disciplines. Team members include a registered paediatric dietitian who coordinates the diet programme; a paediatric neurologist who is experienced in offering the ketogenic diet; and a registered nurse who is familiar with childhood epilepsy. Additional help may come from a medical social workerwho works with the family and a pharmacist who can advise on the carbohydrate content of medicines. Lastly, the parents and other caregivers must be educated in many aspects of the diet for it to be safely implemented.[5]

Implementing the diet can present difficulties for caregivers and the patient due to the time commitment involved in measuring and planning meals. Since any unplanned eating can potentially break the nutritional balance required, some people find the discipline needed to maintain the diet challenging and unpleasant. Some people terminate the diet or switch to a less demanding diet, like the modified Atkins diet (MAD) or the low-glycaemic index treatment (LGIT) diet, because they find the difficulties too great.[42]

Initiation

The Johns Hopkins Hospital protocol for initiating the ketogenic diet has been widely adopted.[43] It involves a consultation with the patient and their caregivers and, later, a short hospital admission.[21] Because of the risk of complications during ketogenic diet initiation, most centres begin the diet under close medical supervision in the hospital.[9]

At the initial consultation, patients are screened for conditions that may contraindicate the diet. A dietary history is obtained and the parameters of the diet selected: the ketogenic ratio of fat to combined protein and carbohydrate, the calorie requirements and the fluid intake.[21]

The day before admission to hospital, the proportion of carbohydrate in the diet may be decreased and the patient begins fasting after his or her evening meal.[21] On admission, only calorie- and caffeine-free fluids[37] are allowed until dinner, which consists of “eggnog[Note 8] restricted to one-third of the typical calories for a meal. The following breakfast and lunch are similar, and on the second day, the “eggnog” dinner is increased to two-thirds of a typical meal’s caloric content. By the third day, dinner contains the full calorie quota and is a standard ketogenic meal (not “eggnog”). After a ketogenic breakfast on the fourth day, the patient is discharged. Where possible, the patient’s current medicines are changed to carbohydrate-free formulations.[21]

When in the hospital, glucose levels are checked several times daily and the patient is monitored for signs of symptomatic ketosis (which can be treated with a small quantity of orange juice). Lack of energy and lethargy are common but disappear within two weeks.[20] The parents attend classes over the first three full days, which cover nutrition, managing the diet, preparing meals, avoiding sugar and handling illness.[21] The level of parental education and commitment required is higher than with medication.[44]

Variations on the Johns Hopkins protocol are common. The initiation can be performed using outpatient clinics rather than requiring a stay in hospital. Often there is no initial fast (fasting increases the risk of acidosis and hypoglycaemia and weight loss). Rather than increasing meal sizes over the three-day initiation, some institutions maintain meal size but alter the ketogenic ratio from 2:1 to 4:1.[9]

For patients who benefit, half achieve a seizure reduction within five days (if the diet starts with an initial fast of one to two days), three-quarters achieve a reduction within two weeks, and 90% achieve a reduction within 23 days. If the diet does not begin with a fast, the time for half of the patients to achieve an improvement is longer (two weeks) but the long-term seizure reduction rates are unaffected.[44] Parents are encouraged to persist with the diet for at least three months before any final consideration is made regarding efficacy.[9]

Maintenance

After initiation, the child regularly visits the hospital outpatient clinic where he or she is seen by the dietitian and neurologist, and various tests and examinations are performed. These are held every three months for the first year and then every six months thereafter. Infants under one year old are seen more frequently, with the initial visit held after just two to four weeks.[9] A period of minor adjustments is necessary to ensure consistent ketosis is maintained and to better adapt the meal plans to the patient. This fine-tuning is typically done over the telephone with the hospital dietitian[21] and includes changing the number of calories, altering the ketogenic ratio, or adding some MCT or coconut oils to a classic diet.[3] Urinary ketone levels are checked daily to detect whether ketosis has been achieved and to confirm that the patient is following the diet, though the level of ketones does not correlate with an anticonvulsant effect.[21] This is performed using ketone test strips containing nitroprusside, which change colour from buff-pink to maroon in the presence of acetoacetate (one of the three ketone bodies).[45]

A short-lived increase in seizure frequency may occur during illness or if ketone levels fluctuate. The diet may be modified if seizure frequency remains high, or the child is losing weight.[21] Loss of seizure-control may come from unexpected sources. Even “sugar-free” food can contain carbohydrates such as maltodextrinsorbitolstarch and fructose. The sorbitol content of suntan lotion and other skincare products may be high enough for some to be absorbed through the skin and thus negate ketosis.[32]

Discontinuation

About 20% of children on the ketogenic diet achieve freedom from seizures, and many are able to reduce the use of anticonvulsant drugs or eliminate them altogether.[3] Commonly, at around two years on the diet, or after six months of being seizure-free, the diet may be gradually discontinued over two or three months. This is done by lowering the ketogenic ratio until urinary ketosis is no longer detected, and then lifting all calorie restrictions.[46] This timing and method of discontinuation mimics that of anticonvulsant drug therapy in children, where the child has become seizure free. When the diet is required to treat certain metabolic diseases, the duration will be longer. The total diet duration is up to the treating ketogenic diet team and parents; durations up to 12 years have been studied and found beneficial.[9]

Children who discontinue the diet after achieving seizure freedom have about a 20% risk of seizures returning. The length of time until recurrence is highly variable but averages two years. This risk of recurrence compares with 10% for resective surgery (where part of the brain is removed) and 30–50% for anticonvulsant therapy. Of those that have a recurrence, just over half can regain freedom from seizures either with anticonvulsants or by returning to the ketogenic diet. Recurrence is more likely if, despite seizure freedom, an electroencephalogram (EEG) shows epileptiform spikes, which indicate epileptic activity in the brain but are below the level that will cause a seizure. Recurrence is also likely if an MRI scan shows focal abnormalities (for example, as in children with tuberous sclerosis). Such children may remain on the diet longer than average, and it has been suggested that children with tuberous sclerosis who achieve seizure freedom could remain on the ketogenic diet indefinitely.[46]

Variants

Classic

A series of four pie charts for the typical American diet, the induction phase of the Atkins diet, the classic ketogenic diet and the MCD ketogenic diet. The typical American diet has about half its calories from carbohydrates where the others have very little carbohydrate. The Atkins diet is higher in protein than the others. Most of the fat in the MCT diet comes from MCT oil.

The ratio of calorific contributions from food components of four diets, by weight

The ketogenic diet is calculated by a dietitian for each child. Age, weight, activity levels, culture and food preferences all affect the meal plan. First, the energy requirements are set at 80–90% of the recommended daily amounts (RDA) for the child’s age (the high-fat diet requires less energy to process than a typical high-carbohydrate diet). Highly active children or those with muscle spasticity require more calories than this; immobile children require less. The ketogenic ratio of the diet compares the weight of fat to the combined weight of carbohydrate and protein. This is typically 4:1, but children who are younger than 18 months, older than 12 years, or who are obese may be started on a 3:1 ratio. Fat is energy-rich, with 9 kcal/g (38 kJ/g) compared to 4 kcal/g (17 kJ/g) for carbohydrate or protein, so portions on the ketogenic diet are smaller than normal. The quantity of fat in the diet can be calculated from the overall energy requirements and the chosen ketogenic ratio. Next, the protein levels are set to allow for growth and body maintenance, and are around 1 g protein for each kg of body weight. Lastly, the amount of carbohydrate is set according to what allowance is left while maintaining the chosen ratio. Any carbohydrate in medications or supplements must be subtracted from this allowance. The total daily amount of fat, protein and carbohydrate is then evenly divided across the meals.[37]

A computer program such as KetoCalculator may be used to help generate recipes.[47] The meals often have four components: heavy whipping cream, a protein-rich food (typically meat), a fruit or vegetable and a fat such as butter, vegetable oil or mayonnaise. Only low-carbohydrate fruits and vegetables are allowed, which excludes bananas, potatoes, peas and corn. Suitable fruits are divided into two groups based on the amount of carbohydrate they contain, and vegetables are similarly divided into two groups. Foods within each of these four groups may be freely substituted to allow for variation without needing to recalculate portion sizes. For example, cooked broccoli, Brussels sprouts, cauliflower and green beans are all equivalent. Fresh, canned or frozen foods are equivalent, but raw and cooked vegetables differ, and processed foods are an additional complication. Parents are required to be precise when measuring food quantities on an electronic scale accurate to 1 g. The child must eat the whole meal and cannot have extra portions; any snacks must be incorporated into the meal plan. A small amount of MCT oil may be used to help with constipation or to increase ketosis.[37]

The classic ketogenic diet is not a balanced diet and only contains tiny portions of fresh fruit and vegetables, fortified cereals and calcium-rich foods. In particular, the B vitaminscalcium and vitamin D must be artificially supplemented. This is achieved by taking two sugar-free supplements designed for the patient’s age: a multivitamin with minerals and calcium with vitamin D.[3] A typical day of food for a child on a 4:1 ratio, 1,500 kcal (6,300 kJ) ketogenic diet comprises:[29]

  • Breakfast: egg with bacon
    28 g egg, 11 g bacon, 37 g of 36% heavy whipping cream, 23 g butter and 9 g apple.
  • Snack: peanut butter ball
    6 g peanut butter and 9 g butter.
  • Lunch: tuna salad
    28 g tuna fish, 30 g mayonnaise, 10 g celery, 36 g of 36% heavy whipping cream and 15 g lettuce.
  • Snack: keto yogurt
    18 g of 36% heavy whipping cream, 17 g sour cream, 4 g strawberries and artificial sweetener.
  • Dinner: cheeseburger (no bun)
    22 g minced (ground) beef, 10 g American cheese, 26 g butter, 38 g cream, 10 g lettuce and 11 g green beans.
  • Snack: keto custard
    25 g of 36% heavy whipping cream, 9 g egg and pure vanilla flavouring.

MCT oil

Normal dietary fat contains mostly long-chain triglycerides (LCT). Medium-chain triglycerides are more ketogenic than LCTs because they generate more ketones per unit of energy when metabolised. Their use allows for a diet with a lower proportion of fat and a greater proportion of protein and carbohydrate,[3] leading to more food choices and larger portion sizes.[4] The original MCT diet developed by Peter Huttenlocher in the 1970s derived 60% of its calories from MCT oil.[18] Consuming that quantity of MCT oil caused abdominal cramps, diarrhoea and vomiting in some children. A figure of 45% is regarded as a balance between achieving good ketosis and minimising gastrointestinal complaints. The classical and modified MCT ketogenic diets are equally effective and differences in tolerability are not statistically significant.[9] The MCT diet is less popular in the United States; MCT oil is more expensive than other dietary fats and is not covered by insurance companies.[3]

Modified Atkins

First reported in 2003, the idea of using a form of the Atkins diet to treat epilepsy came about after parents and patients discovered that the induction phase of the Atkins diet controlled seizures. The ketogenic diet team at Johns Hopkins Hospital modified the Atkins diet by removing the aim of achieving weight loss, extending the induction phase indefinitely, and specifically encouraging fat consumption. Compared with the ketogenic diet, the modified Atkins diet (MAD) places no limit on calories or protein, and the lower overall ketogenic ratio (approximately 1:1) does not need to be consistently maintained by all meals of the day. The MAD does not begin with a fast or with a stay in hospital and requires less dietitian support than the ketogenic diet. Carbohydrates are initially limited to 10 g per day in children or 20 g per day in adults, and are increased to 20–30 g per day after a month or so, depending on the effect on seizure control or tolerance of the restrictions. Like the ketogenic diet, the MAD requires vitamin and mineral supplements and children are carefully and periodically monitored at outpatient clinics.[48]

The modified Atkins diet reduces seizure frequency by more than 50% in 43% of patients who try it and by more than 90% in 27% of patients.[3] Few adverse effects have been reported, though cholesterol is increased and the diet has not been studied long term.[48] Although based on a smaller data set (126 adults and children from 11 studies over five centres), these results from 2009 compare favourably with the traditional ketogenic diet.[3]

Low glycaemic index treatment

The low glycaemic index treatment (LGIT)[49] is an attempt to achieve the stable blood glucose levels seen in children on the classic ketogenic diet while using a much less restrictive regimen. The hypothesis is that stable blood glucose may be one of the mechanisms of action involved in the ketogenic diet,[9] which occurs because the absorption of the limited carbohydrates is slowed by the high fat content.[5] Although it is also a high-fat diet (with approximately 60% calories from fat),[5] the LGIT allows more carbohydrate than either the classic ketogenic diet or the modified Atkins diet, approximately 40–60 g per day.[3] However, the types of carbohydrates consumed are restricted to those that have a glycaemic index lower than 50. Like the modified Atkins diet, the LGIT is initiated and maintained at outpatient clinics and does not require precise weighing of food or intensive dietitian support. Both are offered at most centres that run ketogenic diet programmes, and in some centres they are often the primary dietary therapy for adolescents.[9]

Short-term results for the LGIT indicate that at one month approximately half of the patients experience a greater than 50% reduction in seizure frequency, with overall figures approaching that of the ketogenic diet. The data (coming from one centre’s experience with 76 children up to the year 2009) also indicate fewer side effects than the ketogenic diet and that it is better tolerated, with more palatable meals.[3][50]

Prescribed formulations

A cream-coloured powder is poured from a tin into a measuring jug on an electronic kitchen scale.

Measuring KetoCal—a powdered formula for administering the classic ketogenic diet

Infants and patients fed via a gastrostomy tube can also be given a ketogenic diet. Parents make up a prescribed powdered formula, such as KetoCal, into a liquid feed.[21] Gastrostomy feeding avoids any issues with palatability, and bottle-fed infants readily accept the ketogenic formula.[32] Some studies have found this liquid feed to be more efficacious and associated with lower total cholesterol than a solid ketogenic diet.[3] KetoCal is a nutritionally complete food containing milk protein and is supplemented with amino acids, fat, carbohydrate, vitamins, minerals and trace elements. It is used to administer the 4:1 ratio classic ketogenic diet in children over one year. The formula is available in both 3:1 and 4:1 ratios, either unflavoured or in an artificially sweetened vanilla flavour and is suitable for tube or oral feeding.[51] Other formula products include KetoVolve[52] and Ketonia.[53] Alternatively, a liquid ketogenic diet may be produced by combining Ross Carbohydrate Free soy formula with Microlipid and Polycose.[53]

Worldwide

There are theoretically no restrictions on where the ketogenic diet might be used, and it can cost less than modern anticonvulsants. However, fasting and dietary changes are affected by religious and cultural issues. A culture where food is often prepared by grandparents or hired help means more people must be educated about the diet. When families dine together, sharing the same meal, it can be difficult to separate the child’s meal. In many countries, food labelling is not mandatory so calculating the proportions of fat, protein and carbohydrate is difficult. In some countries, it may be hard to find sugar-free forms of medicines and supplements, to purchase an accurate electronic scale, or to afford MCT oils.[54]

In Asia, the normal diet includes rice and noodles as the main energy source, making their elimination difficult. Therefore, the MCT-oil form of the diet, which allows more carbohydrate, has proved useful. In India, religious beliefs commonly affect the diet: some patients are vegetarians, will not eat root vegetables or avoid beef. The Indian ketogenic diet is started without a fast due to cultural opposition towards fasting in children. The low-fat, high-carbohydrate nature of the normal Indian and Asian diet means that their ketogenic diets typically have a lower ketogenic ratio (1:1) than in America and Europe. However, they appear to be just as effective.[54]

In many developing countries, the ketogenic diet is expensive because dairy fats and meat are more expensive than grain, fruit and vegetables. The modified Atkins diet has been proposed as a lower-cost alternative for those countries; the slightly more expensive food bill can be offset by a reduction in pharmaceutical costs if the diet is successful. The modified Atkins diet is less complex to explain and prepare and requires less support from a dietitian.[55]

Mechanism of action[edit]

Seizure pathology[edit]

The brain is composed of a network of neurons that transmit signals by propagating nerve impulses. The propagation of this impulse from one neuron to another is typically controlled by neurotransmitters, though there are also electrical pathways between some neurons. Neurotransmitters can inhibit impulse firing (primarily done by γ-aminobutyric acid, or GABA) or they can excite the neuron into firing (primarily done by glutamate). A neuron that releases inhibitory neurotransmitters from its terminals is called an inhibitory neuron, while one that releases excitatory neurotransmitters is an excitatory neuron. When the normal balance between inhibition and excitation is significantly disrupted in all or part of the brain, a seizure can occur. The GABA system is an important target for anticonvulsant drugs, since seizures may be discouraged by increasing GABA synthesis, decreasing its breakdown, or enhancing its effect on neurons.[11]

The nerve impulse is characterised by a great influx of sodium ions through channels in the neuron’s cell membrane followed by an efflux of potassium ions through other channels. The neuron is unable to fire again for a short time (known as the refractory period), which is mediated by another potassium channel. The flow through these ion channels is governed by a “gate” which is opened by either a voltage change or a chemical messenger known as a ligand (such as a neurotransmitter). These channels are another target for anticonvulsant drugs.[11]

There are many ways in which epilepsy occurs. Examples of pathological physiology include: unusual excitatory connections within the neuronal network of the brain; abnormal neuron structure leading to altered current flow; decreased inhibitory neurotransmitter synthesis; ineffective receptors for inhibitory neurotransmitters; insufficient breakdown of excitatory neurotransmitters leading to excess; immature synapse development; and impaired function of ionic channels.[11]

Seizure control

Although many hypotheses have been put forward to explain how the ketogenic diet works, it remains a mystery. Disproven hypotheses include systemic acidosis (high levels of acid in the blood), electrolyte changes and hypoglycaemia (low blood glucose).[21] Although many biochemical changes are known to occur in the brain of a patient on the ketogenic diet, it is not known which of these has an anticonvulsant effect. The lack of understanding in this area is similar to the situation with many anticonvulsant drugs.[56]

On the ketogenic diet, carbohydrates are restricted and so cannot provide for all the metabolic needs of the body. Instead, fatty acids are used as the major source of fuel. These are used through fatty-acid oxidation in the cell’s mitochondria (the energy-producing parts of the cell). Humans can convert some amino acids into glucose by a process called gluconeogenesis, but cannot do this for fatty acids.[57] Since amino acids are needed to make proteins, which are essential for growth and repair of body tissues, these cannot be used only to produce glucose. This could pose a problem for the brain, since it is normally fuelled solely by glucose, and most fatty acids do not cross the blood–brain barrier. Fortunately, the liver can use long-chain fatty acids to synthesise the three ketone bodies β-hydroxybutyrateacetoacetate and acetone. These ketone bodies enter the brain and substitute for glucose.[56] Medium-chain fatty acids octonoic and heptanoic acids can cross the barrier and be used by the brain.[58][59][60]

The ketone bodies are possibly anticonvulsant in themselves; in animal models, acetoacetate and acetone protect against seizures. The ketogenic diet results in adaptive changes to brain energy metabolism that increase the energy reserves; ketone bodies are a more efficient fuel than glucose, and the number of mitochondria is increased. This may help the neurons to remain stable in the face of increased energy demand during a seizure, and may confer a neuroprotective effect.[56]

The ketogenic diet has been studied in at least 14 rodent animal models of seizures. It is protective in many of these models and has a different protection profile than any known anticonvulsant. Conversely, fenofibrate, not used clinically as an antiepileptic, exhibits experimental anticonvulsant properties in adult rats comparable to the ketogenic diet.[61] This, together with studies showing its efficacy in patients who have failed to achieve seizure control on half a dozen drugs, suggests a unique mechanism of action.[56]

Anticonvulsants suppress epileptic seizures, but they neither cure nor prevent the development of seizure susceptibility. The development of epilepsy (epileptogenesis) is a process that is poorly understood. A few anticonvulsants (valproatelevetiracetam and benzodiazepines) have shown antiepileptogenic properties in animal models of epileptogenesis. However, no anticonvulsant has ever achieved this in a clinical trial in humans. The ketogenic diet has been found to have antiepileptogenic properties in rats.[56]

Recently, a saturated medium-chain fatty acid called decanoic acid (C10) has shown promise in both the control of seizures and of neurodegeneration. Decanoic acid is a major constituent of the MCT ketogenic diet, and the authors suggest its action may be through inducing mitochondrial biogenesis and helping provide more ATP to maintain the resting membrane potential of the neuron.[62]

Other applications

The ketogenic diet may be a successful treatment for several rare metabolic diseases. Case reports of two children indicate that it may be a possible treatment for astrocytomas, a type of brain tumour. Autismdepressionmigraine headaches, polycystic ovary syndrome and diabetes mellitus type 2 have also been shown to improve in small case studies.[21] There is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including amyotrophic lateral sclerosisAlzheimer’s disease and Parkinson’s disease,[21][63] and may be protective in traumatic brain injury and stroke.[7][8]

Because tumor cells are inefficient in processing ketone bodies for energy, the ketogenic diet has also been suggested as a treatment for cancer,[64][65] including glioma,[66] as well as multiple sclerosis and other neurological disorders.[67][68]

A 2013 review said that there is enough suggestion of potential benefit from ketogenic diets in cancer therapy that establishing clinical trials is probably warranted.[69] At present the only evidence of benefit is anecdotal, but designing effective trials to measure the effect of adopting a ketogenic diet could prove challenging.[70]

See also

Notes

  1. Jump up^ In this article, kcal stands for calories as a unit of measure (4.1868 kJ), and calories stands for “energy” from food.
  2. Jump up^ Unless otherwise stated, the term fasting in this article refers to going without food while maintaining calorie-free fluid intake.
  3. Jump up^ Hippocrates, On the Sacred Disease, ch. 18; vol. 6.
  4. Jump up^ Hippocrates, Epidemics, VII, 46; vol. 5.
  5. Jump up^ Galen, De venae sect. adv. Erasistrateos Romae degentes, c. 8; vol. 11.
  6. Jump up^ Galen, De victu attenuante, c. 1.
  7. Jump up^ good reduction is defined here to mean a 50–90% decrease in seizure frequency. An excellent reduction is a 90–99% decrease.
  8. Jump up^ Ketogenic “eggnog” is used during induction and is a drink with the required ketogenic ratio. For example, a 4:1 ratio eggnog would contain 60 g of 36% heavy whipping cream, 25 g pasteurised raw egg, saccharin and vanilla flavour. This contains 245 kcal (1,025 kJ), 4 g protein, 2 g carbohydrate and 24 g fat (24:6 = 4:1).[20] The eggnog may also be cooked to make a custard, or frozen to make ice cream.[37]

References

https://en.wikipedia.org/wiki/Ketogenic_diet

Read Full Post | Make a Comment ( None so far )

Electrolytes — Body Type — Diet — Sleep More — Less Stress — Exercise — Fast — Videos

Posted on October 29, 2017. Filed under: American History, Beef, Biology, Blogroll, Books, Bread, Business, Chemistry, College, Communications, Computers, Congress, Crisis, Diet, Diet, Disease, Documentary, Education, Energy, Environment, Exercise, Family, Famine, Farming, Food, Freedom, Friends, Fruit, Geology, government spending, Health, Health Care, history, Language, Law, liberty, Life, Links, Literacy, Love, media, Medical, Medicine, Milk, Money, Non-Fiction, Philosophy, Photos, Physics, Political Correctness, Politics, Press, Psychology, Rants, Raves, Raymond Thomas Pronk, Regulations, Resources, Reviews, Science, Security, Sleep, Speech, Sports, Strategy, Stress Reduction, Success, Talk Radio, Technology, Trade, Unemployment, Vegetables, Video, Water, Wealth, Welfare, Wisdom, Work, Writing | Tags: , , , , , , , , , , , , , , , , , , , , , , , |

Image result for electolitesImage result for electolitesImage result for electolites

Image result for electolitesImage result for electolites

Image result for electolites

Image result for electolites

Image result for electolites

Image result for electolites

Image result for electolites

Breaking Bad Battery

Fluid and Electrolytes: Everything You Need to Know!

Fluids & Electrolytes Made Simple

What Is An Electrolyte?

The 4 Electrolytes and their Symptoms When Losing Weight

POTASSIUM: The MOST Important Electrolyte – MUST WATCH!

The Top Symptoms of a Potassium Deficiency

Potassium & Blood Pressure: MUST WATCH!

How to Fix a Slow Metabolism: MUST WATCH!

How to Fix Urination at Night (Nocturia)? MUST WATCH!

What Urine Color Indicates About Your Body

Why Does My Urine Have a Strong Stinky Odor?

Electrolyte Imbalance Signs & Symptoms: Sweet and Simple

Belly Swelling & Bloating as the Day Progresses?

How to Reduce BLOATING Quickly

#1 Top Food to Burn Belly Fat Tip

The Best Time to Eat to Lose Weight

The 10 Causes of Inflammation

Stop the 5 Causes of Inflammation: FAST!

Deeper Causes of Pain and Inflammation – by Dr. Eric Berg DC

My Theory on Dementia, Blood Pressure & Stroke – Dr. Eric Berg DC

Why Vitamin K2 is so important (and how to get it)

Can Vitamin K2 Fix Cavities

Clogged Arteries, Osteoporosis and Vitamin K2 – Dr. Eric Berg DC

Dr. Berg’s Vitamin K2: and how to use it

The Best Vitamin K2 Foods

Vitamin D3 and K2 Facts ~ Why you need vitamin D3 and K2 in a supplement

Hypertension and Vitamin K2 & D3 Testimonial – Dr. Eric Berg DC

Vitamin K2 Sources and its Health Benefits

Should I Supplement Vitamin K2?

How To Get Vitamin K2

Vitamin K2 & What It Does – Calcium Metabolism – Dr. Eric Berg DC

Drop 1 SIZE In 1 Week GUARANTEED!

What Are The 4 Body Types?

What to Eat for Your Body Type?

Body Type l What Is My Shape l How to Find Your Body Type l Mesomorph l Take the Quiz

What Body Type and Belly Shape Are You? How Hormones Distort The Way Look

How To Fix Your Adrenal Body Type

Published on Apr 29, 2017

http://bit.ly/AdrenalBodyTypeKit Take Dr. Berg’s Advanced Evaluation Quiz: http://bit.ly/EvalQuiz Your report will then be sent via email analyzing 104 potential symptoms, giving you a much deeper insight into the cause-effect relationship of your body issues. It’s free and very enlightening. Dr. Berg talks about the Adrenal Body Type. This type has a series of symptoms: 1. Belly Fat 2. Low tolerance to stress 3. Asthma 4. Allergies 5. High blood pressure 6. Low vitamin D 7. Buffalo hump 8. Diabetes 9. Inflammation 10. Acid reflux Here’s what to do: 1. Low intensity exercise 2. Sleep more 3. No sugar 4. Lots of greens (7-10 cups of vegetables) 5. Protein 3-6oz 6. The Adrenal Body Type Kit Dr. Eric Berg DC Bio: Dr. Berg, 51 years of age is a chiropractor who specializes in weight loss through nutritional and natural methods. His private practice is located in Alexandria, Virginia. His clients include senior officials in the U.S. government and the Justice Department, ambassadors, medical doctors, high-level executives of prominent corporations, scientists, engineers, professors, and other clients from all walks of life. He is the author of The 7 Principles of Fat Burning, published by KB Publishing in January 2011. Dr. Berg trains chiropractors, physicians and allied healthcare practitioners in his methods, and to date he has trained over 2,500 healthcare professionals. He has been an active member of the Endocrinology Society, and has worked as a past part-time adjunct professor at Howard University. DR. BERG’S VIDEO BLOG: http://www.drberg.com/blog FACEBOOK: http://www.facebook.com/DrEricBerg TWITTER: http://twitter.com/DrBergDC YOUTUBE: https://www.youtube.com/user/drericbe… ABOUT DR. BERG: http://www.drberg.com/dr-eric-berg/bio DR. BERG’S SEMINARS: http://www.drberg.com/seminars DR. BERG’S STORY: http://www.drberg.com/dr-eric-berg/story DR. BERG’S CLINIC: https://www.drberg.com/dr-eric-berg/c… DR. BERG’S HEALTH COACHING TRAINING: http://www.drberg.com/weight-loss-coach DR. BERG’S SHOP: http://shop.drberg.com/ DR. BERG’S REVIEWS: http://www.drberg.com/reviews

What To Do If You Have Adrenal Fatigue

Improve Your Sleep With Acupressure / Reduce Adrenal Stress To Get a Restful Sleep

Breathing Exercises For Sleep

How to Sleep Super Fast – MUST WATCH!

Can’t Sleep? DO THIS!

 

Dr. Berg Scheduled to Do the Dr. Oz Show…Then THIS Happens! MUST WATCH

How Dr. Oz Disappointed Us With His Double Life

Read Full Post | Make a Comment ( None so far )

The Weight of America — America’s Number 1 Health Crisis –The Art of The Meal — President Trump Is Not Obese, Trump Is Fluffy — Videos

Posted on October 24, 2017. Filed under: American History, Blogroll, Diet, Exercise, Health, Health Care, history, Law, liberty, Life, Links, Obamacare, Radio, Sleep, Stress Reduction, Television | Tags: , , , , , , , , |

Image result for weight of america

Image result for weight of america

Image result for weight of america

Image result for BMI Body Mass Index

Image result for BMI Body Mass Index

Image result for weight of america

The Weight of the Nation: Part 1 – Consequences (HBO Docs)

The Weight of the Nation: Part 2 – Choices (HBO Docs)

The Weight of the Nation: Part 3 – Children in Crisis (HBO Docs)

The Weight of the Nation: Part 3 – Challenges (HBO Docs)

How to Calculate Body Mass Index

Donald Trump Health Stats Reveal His Body Mass Index Is Just Under Obese

The Art of the Meal | Real Time with Bill Maher (HBO)

Gabriel Iglesias Stand Up Comedy – Gabriel Iglesias Hot and Fluffy 2017

“The President” – Gabriel Iglesias (from my I’m Not Fat… I’m Fluffy comedy special)

Gabriel Iglesias | I’M NOT FAT, I’M FLUFFY Stand Up Special Show

Fluffy Visits Saudi Arabia – Gabriel Iglesias (from Aloha Fluffy: Gabriel Iglesias Live from Hawaii)

 

Read Full Post | Make a Comment ( None so far )

America’s Addiction: Sugar Sugar–Pure White and Deadly–Fructose Is Poison–Are You A Sugar Addict?–Videos

Posted on February 28, 2012. Filed under: American History, Blogroll, Business, Communications, Economics, Education, Federal Government, government, government spending, Health Care, history, Law, liberty, Life, Links, media, People, Philosophy, Politics, Taxes, War, Wealth, Wisdom | Tags: , , , , , , , , , , , , , |

The Archies – Sugar Sugar (’69)

Sugar, Oh, Honey Honey.

 You are my candy girl, and you got me wanting you.

 Honey, Oh, Sugar, Sugar.

You are my candy girl and you got me wanting you.

I just can’t believe the loveliness of loving you.

 (I just can’t believe it’s true).

 I just can’t believe the wonder of this feeling too.

(I just can’t believe it’s true).

Sugar, Oh, Honey Honey.

You are my candy girl, and you got me wanting you.

Honey, Oh, Sugar, Sugar.

You are my candy girl and you got me wanting you.

When I kissed you girl, I knew how sweet a kiss could be.

(I know how sweet a kiss can be)

Like the summer sunshine pour your sweetness over me.

 (Pour your sweetness over me).

Oh pour little sugar on me honey (sugar)

Pour little sugar on me baby (honey honey)

When you make love so sweet (Yeah Yeah Yeah.)

Pour little sugar on me (oh yeah)

Pour little sugar on me honey

 Pour little sugar on me baby I’m gonna make love so sweet (hey hey hey)

Pour little sugar on me honey.

Ah sugar. Oh honey, honey.

 You are my candy, girl, and you got me wanting you.

Oh honey (honey, honey, sugar, sugar)

 Sugar, sugar You are my candy girl.

source: http://www.lyricsondemand.com/

High Fructose Corn Syrup 

Robert “Sugar: Bitter Truth” Lustig on ABCNews

Big Sugar

http://topdocumentaryfilms.com/big-sugar/

Before Lustig’s Bitter Truth – The Sugar Trap – 1986 – 1 of 6 – Documentary

Before Lustig’s Bitter Truth – The Sugar Trap – 1986 – 2 of 6 – Documentary

Before Lustig’s Bitter Truth – The Sugar Trap – 1986 – 3 of 6 – Documentary

Before Lustig’s Bitter Truth – The Sugar Trap – 1986 – 4 of 6 – Documentary

Before Lustig’s Bitter Truth – The Sugar Trap – 1986 – 5 of 6 – Documentary

Before Lustig’s Bitter Truth – The Sugar Trap – 1986 – 6 of 6 – Documentary

The Politics of Obesity – Freedomain Radio Interviews Dr. Robert H. Lustig 

Sugar: The Bitter Truth- March 24, 2011

Sugar: The Bitter Truth 

Robert H. Lustig, MD, UCSF Professor of Pediatrics in the Division of Endocrinology, explores the damage caused by sugary foods. He argues that fructose (too much) and fiber (not enough) appear to be cornerstones of the obesity epidemic through their effects on insulin. Series: UCSF Mini Medical School for the Public [7/2009] [Health and Medicine] [Show ID: 16717]

Sugar: The Bitter Truth (The SHORT Version) 

Are You a Sugar Addict?

DEATH BY SUGAR by Jorge Cruise 

The Sugar Epidemic: Policy versus Politics 

Sugar Dangers – Dr. Richard Johnson Lecture (Part 1 of 3) 

Sugar Dangers – Dr. Richard Johnson Lecture (Part 2 of 3) 

Sugar Dangers – Dr. Richard Johnson Lecture (Part 3 of 3) 

Dr. Mercola Interviews Dr. Richard Johnson on Fructose (Part 1 of 5) 

Dr. Mercola Interviews Dr. Richard Johnson on Fructose (Part 2 of 5)

Dr. Mercola Interviews Dr. Richard Johnson on Fructose (Part 3 of 5)

Dr. Mercola Interviews Dr. Richard Johnson on Fructose (Part 4 of 5)

Dr. Mercola Interviews Dr. Richard Johnson on Fructose (Part 5 of 5)

Dr. Mark’s Minute – High Fructose Corn Syrup is POISON  Reason #1

Dr. Mark’s Minute – High Fructose Corn Syrup is POISON Reason #2

Dr. Mark’s Minute – High Fructose Corn Syrup is POISON: Reason #3

Mark’s Minute – High Fructose Corn Syrup is POISON: Reason #4

SWEET SUICIDE: OR HOW SUGAR RUINS YOUR HEALTH

Conspiracy for Fat America & High-Fructose Corn Syrup

High-Fructose Corn Syrup Truth, Still Not Sexy, HFCS

How much sugar does the average american consume?

The Great Sugar Shaft

Sugar Daddy: Taubes tells all

Larry Graham, Chairman of the Coalition for Sugar Reform, Discusses Need to Reform the Sugar Program

Fran Smith, Board Member & Adjunct Fellow at CEI, on the Economic Impact of the Sugar Program

The Case Against the Sugar Program on CNBC Squawk Box

Sugar

“…Sugar is a class of edible crystalline carbohydrates, mainly sucrose, lactose, and fructose,[1] characterized by a sweet flavor.

Sucrose in its refined form primarily comes from sugar cane and sugar beet. It and the other sugars are present in natural and refined forms in many foods, and the refined forms are also added to many food preparations.

The world produced about 168 million tonnes of sugar in 2011.[2] The world consumed an average of 24 kilograms of sugar for every human being of all ages, equivalent to over 260 food calories per day per human being.[3]

In food, “sugars” refer to all monosaccharides and disaccharides present in food, but excludes polyols,[4] while in its singular form, “sugar” normally refers to sucrose. The other sugars are usually known by more specific names — glucose, fructose or fruit sugar, high fructose corn syrup, etc.

Sugar production and trade has influenced human history in many ways. In modern times, sugar influenced the formation of colonies, perpetuation of slavery, transition to indentured labor, migration and abuse of people, wars between 19th century sugar trade controlling nations, ethnic composition and political structure of the new world.[5][6]

Ancient times and Middle Ages

Sugar has been produced in the Indian subcontinent[7] since ancient times. It was not plentiful or cheap in early times—honey was more often used for sweetening in most parts of the world.

Amongst the ancient manuscripts of China, dated to be from the eight century BC, one of the earliest historical mention of sugar cane is included along with the fact that their knowledge of sugar cane was derived from India.[8] It appears that in about 500 BC, residents of present-day India began making sugar syrup and cooling it in large flat bowls to make crystals that were easier to store and transport. In the local Indian language, these crystals were called khanda (खण्ड), which is the source of the word candy.[9]

Originally, people chewed sugarcane raw to extract its sweetness. Sugarcane was a native of tropical South Asia and Southeast Asia.[10] Different species likely originated in different locations with Saccharum barberi originating in India and S. edule and S. officinarum coming from New Guinea.[10][11]

Sugar remained relatively unimportant until the Indians discovered methods of turning sugarcane juice into granulated crystals that were easier to store and to transport.[12] Crystallized sugar was discovered by the time of the Imperial Guptas, around 5th century AD.[12] Indian sailors, consumers of clarified butter and sugar, carried sugar by various trade routes.[12] Traveling Buddhist monks brought sugar crystallization methods to China.[13] During the reign of Harsha (r. 606–647) in North India, Indian envoys in Tang China taught sugarcane cultivation methods after Emperor Taizong of Tang (r. 626–649) made his interest in sugar known, and China soon established its first sugarcane cultivation in the seventh century.[14] Chinese documents confirm at least two missions to India, initiated in 647 AD, for obtaining technology for sugar-refining.[15] In South Asia, the Middle East and China, sugar became a staple of cooking and desserts.

The triumphant progress of Alexander the Great was halted on the banks of river Indus by the refusal of his troops to go further east. They saw people in the Indian subcontinent growing sugarcane and making granulated, salt-like sweet powder, locally called साखर, pronounced as saccharum (ζάκχαρι). On their return journey, the Macedonian soldiers carried the “honey bearing reeds.” Sugarcane remained a limited crop for over a millennium, sugar a rare commodity, and traders of sugar wealthy. Venice, at the height of its financial power, was the chief sugar-distributing center of Europe.[8]

Crusaders brought sugar home with them to Europe after their campaigns in the Holy Land, where they encountered caravans carrying “sweet salt”. Early in the 12th century, Venice acquired some villages near Tyre and set up estates to produce sugar for export to Europe, where it supplemented honey as the only other available sweetener.[16] Crusade chronicler William of Tyre, writing in the late 12th century, described sugar as “very necessary for the use and health of mankind”.[17]

Modern history

In August 1492, Christopher Columbus stopped at La Gomera in the Canary Islands, for wine and water, intending to stay only four days. He became romantically involved with the Governor of the island, Beatriz de Bobadilla y Ossorio, and stayed a month. When he finally sailed she gave him cuttings of sugarcane, which became the first to reach the New World.

Sugar was a luxury in Europe prior to 18th century. It became widely popular in 18th century, then graduated to becoming a necessity in the 19th century. This evolution of taste and demand for sugar as an essential food ingredient unleashed major economic and social changes.[5] It drove, in part, colonization of tropical islands and nations where labor-intensive sugarcane plantations and sugar manufacturing could thrive. The demand for cheap and docile labor for harsh inhumane work, in part, first drove slave trade from Africa (in particular West Africa), followed by indentured labor trade from South Asia (in particular India).[6][18][19] Millions of slave and indentured laborers were brought into the Caribbean, Indian Ocean, Pacific Islands, East Africa, Natal, north and eastern parts of South America, and southeast Asia. The modern ethnic mix of many nations, settled in last two centuries, has been influenced by sugar.[20][21][22]

Sugar also led to some industrialization of former colonies. For example, Lieutenant J. Paterson, of the Bengal establishment, persuaded British government that sugar cane could be cultivated in British India with many advantages, and at less expense than in the West Indies. As a result, a number of sugar factories were established in Bihar in British India.[23]

More recently it is manufactured in very large quantities in many countries, largely from sugarcane and sugar beet. In processed foods it has increasingly been supplanted by corn syrup.

Etymology

The etymology reflects the spread of the commodity. The English word “sugar”[24] originates from the Arabic word سكر sukkar, itself from the Persian shakar,[25] itself derived from Sanskrit शर्करा sharkara.[26] It most probably came to England by way of Italian merchants. The contemporary Italian word is zucchero, whereas the Spanish and Portuguese words, azúcar and açúcar respectively, have kept a trace of the Arabic definite article. The Old French word is zuchre – contemporary French sucre. The earliest Greek word attested is σάκχαρις (sákkʰaris).[27][28] A satisfactory pedigree explaining the spread of the word has yet to be done. Note that the English word jaggery (meaning “coarse brown Indian sugar”) has similar ultimate etymological origins (presumably in Sanskrit).

Production

The five largest producers of sugar in 2010 were Brazil, India, European Union, China and Thailand. The largest exporters in 2010 were Brazil, Thailand, Australia and India; while the largest importers were EU-27, United States and Indonesia. Currently, Brazil is the highest per capita consumer of sugar, followed by Australia, Thailand and EU-27.[29][30]

Consumption

The per capita consumption of refined sugar in America has varied between 27 to 46 kilograms in the last 40 years. In 2008, American per capita total consumption of sugar and sweeteners – exclusive of artificial sweeteners – equaled 61.9 kilograms per year (136.2 pounds).[31][32]

Sugar is an important component of human food balance. According to FAO, about 24 kilograms of sugar – equivalent to over 260 food calories per day – was, on average, consumed annually per human being of all ages in the world in 1999. Even with rising human population, sugar consumption is expected to increase to 25.1 kilograms per human being by 2015.[3]

Health effects

Some studies involving the health impact of sugars are effectively inconclusive. The WHO and FAO meta studies have shown directly contrasting impacts of sugar in refined and unrefined forms [33] and since most studies do not use a population who are not consuming any “free sugars” at all, the baseline is effectively flawed (or as the report puts it, the studies are “limited”). Hence there are articles such as Consumer Reports on Health that said in 2008, “Some of the supposed dietary dangers of sugar have been overblown. Many studies have debunked the idea that it causes hyperactivity, for example.”[34] though the article does continue to discuss other health impacts of sugar. Other articles and studies refer to the increasing evidence supporting the links to hyperactivity.[35] The WHO FAO meta-study suggests that such results are expected when some studies do not effectively segregate or control for free sugars as opposed to sugars still in their natural form (entirely unrefined) while others do.

Blood glucose levels

Sugar, because of its simpler chemical structure, may raise blood glucose levels more quickly than starch. This finding suggests that this basic differentiation between starch and sugar is insufficient reason to segregate these two substances for controlling blood glucose levels in diabetics, the idea behind carbohydrate counting.[36] A more effective distinction could use that suggested by multiple meta-studies between free sugars and naturally-occurring sugars which do suggest different impacts on health.[33][37]

Obesity and diabetes

Studies appear to conflict with some suggesting eating excessive amounts of sugar does not increase the risk of diabetes, although the extra calories from consuming large amounts of sugar can lead to obesity, which may increase the risk of diabetes,[38][39][39][40][41][42][42][43] while others show links between refined sugar (free sugar) consumption and the onset of diabetes, and negative correlation with the consumption of fiber[44][45][46][47] including a 2010 meta-analysis of eleven studies involving 310,819 participants and 15,043 cases of type 2 diabetes[48] that found that “SSBs (sugar-sweetened beverages) may increase the risk of metabolic syndrome and type 2 diabetes not only through obesity but also by increasing dietary glycemic load, leading to insulin resistance, β-cell dysfunction, and inflammation”. As an overview to consumption related to chronic disease and obesity, the World Health Organization’s independent meta-studies specifically distinguish free sugars (“all monosaccharides and disaccharides added to foods by the manufacturer, cook or consumer, plus sugars naturally present in honey, syrups and fruit juices”) from sugars naturally present in food. The reports prior to 2000 set the limits for free sugars at a maximum of 10% of carbohydrate intake, measured by energy, rather than mass, and since 2002 [33] have aimed for a level across the entire population at less than 10%. The consultation committee recognized that this goal is “controversial. However, the Consultation considered that the studies showing no effect of free sugars on excess weight have limitations.” (p. 57).

Cardiovascular disease

A number of studies in animals have suggested that chronic consumption of refined sugars can contribute to metabolic and cardiovascular dysregulation. Some experts have suggested that refined fructose is more damaging than refined glucose in terms of cardiovascular risk.[49] Cardiac performance has been shown to be impaired by switching from a carbohydrate diet including fiber to a high-carbohydrate diet.[50]

Switching saturated fatty acids for carbohydrates with high glycemic index values shows a statistically significant positive association with the risk of myocardial infarction.[51]

Other studies have found links between high fat and high glycemic index carbohydrates accelerates the development of cardiac pathology and pump dysfunction in hypertension despite no signs of diabetes and only a modest level of obesity, suggesting that the link between obesity and coronary heart disease should be shifted towards macronutrients and the high glycemic load typical of the “junk-food” diet.[52]

The consumption of added sugars has been positively associated with multiple measures known to increase cardiovascular disease risk amongst adolescents as well as adults.[53]

Studies are suggesting the impact of refined carbohydrates or high glycemic load carbohydrates are more significant that the impact of saturated fatty acids on cardiovascular disease.[54][55]

A high dietary intake of sugar (in this case, sucrose or disaccharide) consumption can substantially increase the risk for heart- and vascular diseases. According to a new Swedish study from Lund University and Malmö University College of 4301 persons, sugar was associated with higher levels of bad blood fat with a high level of small and medium LDL and reduced HDL blood fat. However the amount of fat intake didn’t affect the blood fats. As a side note, moderate quantities of alcohol and protein were linked to the good HDL blood fat.[56]

Alzheimer disease

It is suggested that Alzheimer Disease is linked with the western diet, characterised by excessive dietary intake of sugar, refined carbohydrates (with a high glycaemic index) and animal products (with a high content of saturated fats) and decreased intake of unrefined seeds. There are also prevention hypotheses that address the diet issue with mono-supplements of specific vitamins or drugs that do not show appreciable results.[57]

Dietary pattern analysis, which considers overall eating patterns comparing those with Alzheimer’s disease as compared to healthy controls using factor analysis, gives a major eating pattern for those with Alzheimer’s characterised by a high intake of meat, butter, high-fat dairy products, eggs and refined sugar, while the other major eating pattern for those without Alzheimer’s was characterised by a high intake of grains and vegetables.[58]

One group of experimenters compared a normal rodent diet (19% protein, 5% fat and 60% complex carbohydrate) with free water access against the same diet but with free access to a 10% sucrose solution. Their data underscore the potential role of dietary sugar in the pathogenesis of Alzheimer disease and suggest that controlling the consumption of sugar-sweetened beverages may be an effective way to curtail the risk of developing Alzheimer disease.[59]

Macular degeneration

There are links between free sugar consumption and macular degeneration in older age.[60]

Tooth decay

In regard to contributions to tooth decay, the role of free sugars is also recommended to be below an absolute maximum of 10% of energy intake, with a minimum of zero. There is “convincing evidence from human intervention studies, epidemiological studies, animal studies and experimental studies, for an association between the amount and frequency of free sugars intake and dental caries” while other sugars (complex carbohydrate) consumption is normally associated with a lower rate of dental caries.[37] Lower rates of tooth decay have been seen in individuals with hereditary fructose intolerance.[61]

Terminology

Popular

The term sugar usually refers to sucrose, which is also called “table sugar” or “saccharose.” Sucrose is a white crystalline disaccharide. It is often obtained from sugar cane or sugar beet.[62] Sucrose is the most popular of the various sugars for flavoring, as well as properties (such as mouthfeel, preservation, and texture) of beverages and food.

Chemical

“Sugar” can also be used to refer to water-soluble crystalline carbohydrates with varying sweetness. Sugars include monosaccharides (e.g., glucose, fructose, galactose), disaccharides (e.g., sucrose, lactose, maltose), trisaccharides, and oligosaccharides,[63] in contrast to complex carbohydrates such as polysaccharides. Corn syrup, dextrose, crystalline fructose, and maltose, for example, are used in manufacturing and preparing food.

Baking weight/mass volume relationship

Different culinary sugars have different densities due to differences in particle size and inclusion of moisture.

The Domino Sugar Company has established the following volume to weight conversions:

  • Brown sugar 1 cup = 48 teaspoons ~ 195 g = 6.88 oz
  • Granular sugar 1 cup = 48 teaspoons ~ 200 g = 7.06 oz
  • Powdered sugar 1 cup = 48 teaspoons ~ 120 g = 4.23 oz

Bulk density[64]

  • Dextrose sugar 0.62 g/mL
  • Granulated sugar 0.70 g/mL
  • Powdered sugar 0.56 g/mL
  • Beet sugar 0.80 g/mL

Purity standards

The International Commission for Uniform Methods of Sugar Analysis sets standards for the measurement of the purity of refined sugar, known as ICUMSA numbers; lower numbers indicate a higher level of purity in the refined sugar.[65]

Chemistry

Sucrose: a disaccharide of glucose (left) and fructose (right), important molecules in the body.
Main article: Carbohydrate

Scientifically, sugar loosely refers to a number of carbohydrates, such as monosaccharides, disaccharides, or oligosaccharides. Monosaccharides are also called “simple sugars,” the most important being glucose. Almost all sugars have the formula CnH2nOn (n is between 3 and 7). Glucose has the molecular formula C6H12O6. The names of typical sugars end with “-ose,” as in “glucose”, “dextrose”, and “fructose”. Sometimes such words may also refer to any types of carbohydrates soluble in water. The acyclic mono- and disaccharides contain either aldehyde groups or ketone groups. These carbon-oxygen double bonds (C=O) are the reactive centers. All saccharides with more than one ring in their structure result from two or more monosaccharides joined by glycosidic bonds with the resultant loss of a molecule of water (H2O) per bond.

Monosaccharides in a closed-chain form can form glycosidic bonds with other monosaccharides, creating disaccharides (such as sucrose) and polysaccharides (such as starch). Enzymes must hydrolyze or otherwise break these glycosidic bonds before such compounds become metabolized. After digestion and absorption the principal monosaccharides present in the blood and internal tissues include glucose, fructose, and galactose. Many pentoses and hexoses can form ring structures. In these closed-chain forms, the aldehyde or ketone group remains non-free, so many of the reactions typical of these groups cannot occur. Glucose in solution exists mostly in the ring form at equilibrium, with less than 0.1% of the molecules in the open-chain form.

Natural polymers of sugars

Biopolymers of sugars are common in nature. Through photosynthesis plants produce glucose, which has the formula C6H12O6, and convert it for storage as an energy reserve in the form of other carbohydrates such as starch, or (as in cane and beet) as sucrose (table sugar). Sucrose has the chemical formula C12H22O11. Starch, consisting of two different polymers of glucose, is a readily degradable chemical energy stored by cells, convertible to other types of energy.

Cellulose is a polymer of glucose used by plants as structural component.

DNA and RNA are built up of the sugars ribose and deoxyribose. The sugar in DNA is deoxyribose, and has the formula C5H10O4.

http://en.wikipedia.org/wiki/Sugar

High-fructose corn syrup

“…High-fructose corn syrup (HFCS)—also called glucose-fructose syrup[1][2] in the UK, glucose/fructose[3] in Canada, and high-fructose maize syrup in other countries—comprises any of a group of corn syrups that has undergone enzymatic processing to convert some of its glucose into fructose to produce a desired sweetness. In the United States, consumer foods and products typically use high-fructose corn syrup as a sweetener. It has become very common in processed foods and beverages in the U.S., including breads, cereals, breakfast bars, lunch meats, yogurts, soups and condiments.[4]

According to the USDA, HFCS consists of 24% water, and the rest sugars. The most widely used varieties of high-fructose corn syrup are: HFCS 55 (mostly used in soft drinks), approximately 55% fructose and 42% glucose; and HFCS 42 (used in beverages, processed foods, cereals and baked goods), approximately 42% fructose and 53% glucose.[5][6] HFCS-90, approximately 90% fructose and 10% glucose, is used in small quantities for specialty applications, but primarily is used to blend with HFCS 42 to make HFCS 55.[7]

In the U.S., HFCS is among the sweeteners that have primarily replaced sucrose (table sugar) in the food industry. Factors for this include governmental production quotas of domestic sugar, subsidies of U.S. corn, and an import tariff on foreign sugar; all of which combine to raise the price of sucrose to levels above those of the rest of the world, making HFCS less costly for many sweetener applications. Critics of the extensive use of HFCS in food sweetening argue that the highly processed substance is more harmful to humans than regular sugar, contributing to weight gain by affecting normal appetite functions[8] , and that in some foods HFCS may be a source of mercury, a known neurotoxin.[9][10] The Corn Refiners Association disputes these claims and maintains that HFCS is comparable to table sugar.[11] Studies by the American Medical Association suggest “it appears unlikely that HFCS contributes more to obesity or other conditions than sucrose”, but welcome further independent research on the subject.[12] Further reviews in the clinical literature have disputed the links between HFCS and obesity,[13] diabetes,[14] and metabolic syndrome,[13] and concluded that HFCS is no different from any other sugar in relationship to these diseases.[dubious – discuss] HFCS has been classified generally recognized as safe (GRAS) by the U.S. Food and Drug Administration since 1976.[15]

Use as a replacement for sugar

HFCS replaces sugar in various processed foods in the United States.[16][17] The main reasons for this switch are:

  • Per relative sweetness, HFCS 55 is comparable to table sugar (sucrose), a disaccharide of fructose and glucose.[18]
  • High-fructose corn syrup HFCS 90 is sweeter than sucrose; HFCS 42 is less sweet than sucrose.
  • HFCS is cheaper in the United States as a result of a combination of corn subsidies and sugar tariffs and quotas.[19] Since the mid 1990s, the United States federal government has subsidized corn growers by $40 billion.[20][21]
  • HFCS is easier to blend and transport because it is a liquid.[22]

Comparison to other sweeteners

High-fructose corn syrup
Nutritional value per 100 g (3.5 oz)
Energy 1,176 kJ (281 kcal)
Carbohydrates 76 g
– Dietary fiber 0 g
Fat 0 g
Protein 0 g
Water 24 g
Riboflavin (vit. B2) 0.019 mg (2%)
Niacin (vit. B3) 0 mg (0%)
Pantothenic acid (B5) 0.011 mg (0%)
Vitamin B6 0.024 mg (2%)
Folate (vit. B9) 0 μg (0%)
Vitamin C 0 mg (0%)
Calcium 6 mg (1%)
Iron 0.42 mg (3%)
Magnesium 2 mg (1%)
Phosphorus 4 mg (1%)
Potassium 0 mg (0%)
Sodium 2 mg (0%)
Zinc 0.22 mg (2%)
Shown is for 100 g, roughly 5.25 tbsp. Percentages are relative to US recommendations for adults. Source: USDA Nutrient Database

Cane and beet sugar

Cane sugar and beet sugar are both relatively pure sucrose. While glucose and fructose, which are the two components of HFCS, are monosaccharides, sucrose is a disaccharide composed of glucose and fructose linked together with a relatively weak glycosidic bond. The fact that sucrose, glucose and fructose are unique, distinct molecules complicates the comparison between cane sugar, beet sugar and HFCS. A molecule of sucrose (with a chemical formula of C12H22O11) can be broken down into a molecule of glucose (C6H12O6) plus a molecule of fructose (also C6H12O6 — an isomer of glucose) in a weakly acidic environment by a process called inversion.[23] Sucrose is broken down during digestion into a mixture of 50% fructose and 50% glucose through hydrolysis by the enzyme sucrase. People with sucrase deficiency cannot digest (break down) sucrose and thus exhibit sucrose intolerance.[24]

Fructose is absorbed from the gastrointestinal tract by a different mechanism than that for glucose. Glucose stimulates insulin release from the isolated pancreas, but fructose does not. Fructose is metabolized primarily in the liver. Once inside the liver cell, fructose can enter the pathways that provide glycerol, the backbone for triacylglycerol. The growing dietary amount of fructose that is derived from sucrose or HFCS has raised questions about how children and adults respond to fructose alone or when it is accompanied by glucose.[25]

Honey

Honey is a mixture of different types of sugars, water, and small amounts of other compounds. Honey typically has a fructose/glucose ratio similar to HFCS 55, as well as containing some sucrose and other sugars. Like HFCS, honey contains water and has approximately 3 kcal per gram. Because of its similar sugar profile and lower price, HFCS has been used illegally to “stretch” honey. As a result, checks for adulteration of honey no longer test for higher-than-normal levels of sucrose, which HFCS does not contain, but instead test for small quantities of proteins that can be used to differentiate between HFCS and honey. Consumers should be aware, however, that some honey available in supermarkets contain HFCS or utilized HFCS in its production. Consumer awareness through label-reading is important for those aiming to avoid high-fructose corn syrup. [26]

Production

HFCS was first introduced by Richard O. Marshall and Earl R. Kooi in 1957. They were, however, unsuccessful in making it viable for mass production.[27] The industrial production process and creation was made by Dr. Y. Takasaki at the Agency of Industrial Science and Technology of Ministry of International Trade and Industry of Japan in 1965–1970. Dr. Y. Takasaki is known to many as the creator of HFCS. HFCS was rapidly introduced to many processed foods and soft drinks in the U.S. from about 1975 to 1985.

High-fructose corn syrup is produced by milling corn to produce corn starch, then processing that starch to yield corn syrup, which is almost entirely glucose, and then adding enzymes that change some of the glucose into fructose. The resulting syrup (after enzyme conversion) contains approximately 42% fructose and is HFCS 42. Some of the 42% fructose is then purified to 90% fructose, HFCS 90. To make HFCS 55, the HFCS 90 is mixed with HFCS 42 in the appropriate ratios to form the desired HFCS 55. The enzyme process that changes the 100% glucose corn syrup into HFCS 42 is as follows:

  1. Cornstarch is treated with alpha-amylase to produce shorter chains of sugars called oligosaccharides.
  2. Glucoamylase – which is produced by Aspergillus, species of mold, in a fermentation vat — breaks the sugar chains down even further to yield the simple sugar glucose.
  3. Xylose isomerase (aka glucose isomerase) converts glucose to a mixture of about 42% fructose and 50–52% glucose with some other sugars mixed in.

While inexpensive alpha-amylase and glucoamylase are added directly to the slurry and used only once, the more costly xylose-isomerase is packed into columns and the sugar mixture is then passed over it, allowing it to be used repeatedly until it loses its activity. This 42–43% fructose glucose mixture is then subjected to a liquid chromatography step, where the fructose is enriched to about 90%. The 90% fructose is then back-blended with 42% fructose to achieve a 55% fructose final product. Most manufacturers use carbon adsorption for impurity removal. Numerous filtration, ion-exchange and evaporation steps are also part of the overall process.

The units of measurement for sucrose is degrees Brix (symbol °Bx). Brix is a measurement of the mass ratio of dissolved sucrose to water in a liquid. A 25 °Bx solution has 25 grams of sucrose per 100 grams of solution (25% w/w). Or, to put it another way, there are 25 grams of sucrose and 75 grams of water in the 100 grams of solution. The Brix measurement was introduced by Antoine Brix.

A more universal measurement of sugars, including HFCS, is called dry solids. Dry solids is defined as the mass ratio of dry sugars to the total weight of the sugar solution. Since Brix is based on the refractive index of light against a sucrose molecule it is not accurate when measuring other sugars such as glucose, maltose, and fructose.

When an infrared Brix sensor is used, it measures the vibrational frequency of the sucrose molecules, giving a Brix degrees measurement. This will not be the same measurement as Brix degrees using a density or refractive index measurement, because it will specifically measure dissolved sugar concentration instead of all dissolved solids. When a refractometer is used, it is correct to report the result as “refractometric dried substance” (RDS). One might speak of a liquid as being 20 °Bx RDS. This is a measure of percent by weight of total dried solids and, although not technically the same as Brix degrees determined through an infrared method, renders an accurate measurement of sucrose content, since the majority of dried solids are in fact sucrose.

Recently, an isotopic method for quantifying sweeteners derived from corn and sugar cane was developed which permits measurement of corn syrup- and cane sugar-derived sweeteners in humans, thus allowing dietary assessment of the intake of these substances relative to total intake.[28]

Sweetener consumption patterns

Historical

Before the mass production of fructose since 1957[citation needed], human beings had little dietary exposure to fructose. Fructose was limited to only a few items such as honey, dates, raisins, grapes and apples. The staples of most early diets, meats and most vegetables, contain no fructose.[29]

United States

US sweetener consumption, 1966-2009, in dry pounds. It is apparent from this graph that overall sweetener consumption, and in particular glucose-fructose mixtures, has increased since the introduction of HFCS. Thus, the amount of fructose consumed in the United States has increased since the early 1980s. This would be true whether the added sweetener was HFCS, table sugar, or any other glucose-fructose mixture.[30]

A system of sugar tariffs and sugar quotas imposed in 1977 in the United States significantly increased the cost of imported sugar and U.S. producers sought cheaper sources. High-fructose corn syrup, derived from corn, is more economical because the domestic U.S. prices of sugar are twice the global price[31] and the price of corn is kept low through government subsidies paid to growers.[32][33]

HFCS became an attractive substitute, and is preferred over cane sugar among the vast majority of American food and beverage manufacturers. Soft drink makers such as Coca-Cola and Pepsi use sugar in other nations, but switched to HFCS in the U.S. and Canada in 1984.[34] Large corporations, such as Archer Daniels Midland, lobby for the continuation of government corn subsidies.[35]

Other countries, including Mexico typically use sugar in soft drinks. Some Americans seek out Mexican Coca-Cola in ethnic groceries, because they prefer the taste compared to Coke made with HFCS.[36][37] Kosher for Passover Coca-Cola sold in the U.S. around the Jewish holiday also uses sucrose rather than HFCS and is also highly sought after by people who prefer the original taste.[38]

The average American consumed approximately 37.8 lb (17.1 kg) of HFCS in 2008, versus 46.7 lb (21.2 kg) of sucrose.[39] In countries where HFCS is not used or rarely used, sucrose consumption per person may be higher than in the USA; sucrose consumption per person from various locations is shown below (2002):[40]

  • USA: 32.4 kg (71 lb)
  • EU: 40.1 kg (88 lb)
  • Brazil: 59.7 kg (132 lb)
  • Australia: 56.2 kg (124 lb)

Of course, in terms of total sugars consumed, the figures from countries where HFCS is not used should be compared to the sum of the sucrose and HFCS figures from countries where HFCS consumption is significant.

European Union

In the European Union (EU), HFCS, known as isoglucose or glucose-fructose syrup, is subject to a production quota. In 2005, this quota was set at 303,000 tons; in comparison, the EU produced an average of 18.6 million tons of sugar annually between 1999 and 2001.[41] Wide scale replacement of sugar has not occurred in the EU.

 Japan

In Japan, HFCS consumption accounts for one quarter of total sweetener consumption.[42]

Health effects

Main article: Health effects of high-fructose corn syrup

Health concerns have been raised about high fructose corn syrup, which allege contribution to obesity, cardiovascular disease, diabetes, and non-alcoholic fatty liver disease. A peer-reviewed study in the American Journal of Clinical Nutrition by John S White who is a Consultant in sweeteners, HFCS and sucrose for the Food and Beverage Industry and also has a professional association with the Corn Refiners Association, rejects the HFCS-obesity hypothesis and finds that “[a]lthough examples of pure fructose causing metabolic upset at high concentrations abound, especially when fed as the sole carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same.”[13]

http://en.wikipedia.org/wiki/High-fructose_corn_syrup

Read Full Post | Make a Comment ( None so far )

Health Benefits of Fasting–Video

Posted on December 23, 2010. Filed under: Agriculture, Biology, Blogroll, Communications, Economics, Education, Health Care, Language, Law, liberty, Life, Links, Medicine, People, Philosophy, Raves, Science, Technology, Video, Wisdom | Tags: , , , , , , |

Dr. Alan Goldhamer on Medical Water Fasting #554

 

Difference Between Juice Fasting and Water Fasting #555

 

Challenges with Raw Food with Dr. Alan Goldhamer #556

 

5 Day Water Fast Experiment at True North (Part 2) #630

 

5 Day Water Fast Experiment at True North (Part 2) #631

 

Do You Fast with Distilled Water? (Water Fast Part 3) #632

 

Do You Fast with Distilled Water? (Water Fast Part 4) #633

 

Do You Fast with Distilled Water? (Water Fast Part 5) #634

 

Breaking a Water Fast (Part 6) #635

 

16 Year Headache Gone after Water Fast (Part 7) #636

 

Pain Gone After 41 Day Water Fast (Part 8) #637

 

Rupert Sheldrake: On Fasting

 

Background Articles and Videos

Fasting 

What is fasting?

 Preparation for Your Fast

 Why Fast?

 Activity Level – 
Fasting enhances mental acuity

 – Protein & Fasting Points

 Healing Aiding – 

Elimination of Toxins

 Fasting decreases dependency on authorities
Reactions from Fasting

 Benefits of Fasting

 Healing Crisis

 One Day Fast – 
Going off your Fast

Water Fast

Water Fasting Tips

Fasting Concerns

Reactions from Fasting

SpiritualWeight Loss

 Pre-existing Conditions
Greater Sensitivity

 Master Cleanse

 Juice Fasting

 References/Links – 

Additional Reading

 Disclaimer

“…What is Fasting?
Fasting is a period of abstinence from all food or specific items. Fluids are consumed in sufficient quantity to satisfy thirst and physiologic requirements. During the absence of food, the body will systematically cleanse itself of everything except vital tissue. Starvation will occur only when the body is forced to use vital tissue to survive. Although protein is being used by the body during the fast, a person fasting even 40 days on water will not suffer a deficiency of protein, vitamins, minerals or fatty acids. In the breakdown of unhealthy cells, all essential substances are used and conserved in a most extraordinary manner. There is an unwarranted fear of fasting that strength diminishes from the catabolism of proteins from muscle fibers. Even during long fasts, the number of muscle fibers remains the same. Although the healthy cells may be reduced in size and strength for a time, they remain perfectly sound. …”

http://falconblanco.com/health/fasting.htm

 

What’s the Healthiest Diet?

TrueNorth Health Center

http://www.healthpromoting.com/

 

Read Full Post | Make a Comment ( None so far )

Liked it here?
Why not try sites on the blogroll...