Liz & Glyn Wainwright

Novelist & Scriptwriter shares with a Scientist & Researcher

Liz & Glyn Wainwright

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Zoe Harcombe et al. brilliantly expose the erroneous basis of much official dietary advice.

PDF (Size:82KB) PP. 240-244   DOI: 10.4236/fns.2013.43032

ABSTRACT

Background: Since 1984 UK citizens have been advised to reduce total dietary fat intake to 30% of total energy and saturated fat intake to 10%. The National Institute of Clinical Excellence [NICE] suggests a further benefit for Coronary Heart Disease [CHD] prevention by reducing saturated fat [SFA] intake to 6% – 7% of total energy and that 30,000 lives could be saved by replacing SFAs with Polyunsaturated fats [PUFAs]. Methods: 20 volumes of the Seven Countries Study, the seminal work behind the 1984 nutritional guidelines, were assessed. The evidence upon which the NICE guidance was based was reviewed. Nutritional facts about fat and the UK intake of fat are presented and the impact of macronutrient confusion on public health dietary advice is discussed. Findings: The Seven Countries study classified processed foods, primarily carbohydrates, as saturated fats. The UK government and NICE do the same, listing biscuits, cakes, pastries and savoury snacks as saturated fats. Processed foods should be the target of public health advice but not natural fats, in which the UK diet is deficient. With reference to the macro and micro nutrient composition of meat, fish, eggs, and dairy foods the article demonstrates that dietary trials cannot change one type of fat for another in a controlled study. Interpretation: The evidence suggests that processed food is strongly associated with the increase in obesity, diabetes, CHD, and other modern illness in our society. The macro and micro nutrients found in meat, fish, eggs and dairy products, are vital for human health and consumption of these nutritious foods should be encouraged.

The Wrong Dietary Advice?

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The Academy of Medical Royal Colleges Obesity Initiative was launched at a parliamentary reception.  At this reception I was able to confirm with several members of the Steering Group that the submissions of evidence (Appendix B in their report) clearly identified Dietary Sugar as a major contributor to this epidemic of Obesity which has steadily increased since around 1980. 

This was the time when we were ill-advised to eat less fat and eat more sugar generating carbohydrate foods (McGovern & COMA). Ironically it was also the time when the food industry gave us low fat options by replacing healthy fats with cheap unhealthy sugars. A 35 year obesity epidemic has ensued.

Dietary Fat and cholesterol was never a cause of obesity or heart disease. It was always the dietary Sugar particularly Fructose that did the damage.

There were many notable contributors and I commend the following evidence submission (click on names for links)

Barry Groves

Bjorn Hammarskjold

Stephanie Seneff

Zoe Harcombe

Robert Suchet

Obesity is generated by Sugar

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The brain is only 2% of your body mass but it contains 25% of your cholesterol.  The cholesterol is vital to memory formation (synapses)  and nerve protection (myelin).  Our livers make 2.5g of fresh cholesterol every day to replace the losses.  The liver delivers the brains fresh daily supply of cholesterol to the brain in small lipid droplets known as LDL.  The empties return to the liver known as HDL with various waste products for recycling and disposal.

To get these vital supplies into the brain the LDL droplets have to cross the blood-brain barrier. The particles carry a protein label which is recognised by the receptors.  The brains receptors lock onto the LDL and allow the particles to pass though into the brains astrocyte cells. These astrocytes use the cholesterol  and fats in the care and feeding of the neurons and all is well with our thoughts and memories.

If we consume a lot of sugary products, especially fructose, the receptors become damaged by sugary attachments and fail to work.  The LDL then builds up in the blood and the brain is starved of fat and cholesterol.  All is now not well with our thoughts and memories.

This is a simplification of our biochemical papers on this matter. Other organs like the heart are also affected this way. How is it possible for an educated professionals to go on misleading us by referring to LDL as “Bad Cholesterol”?   

Fructose is getting away with murder and the blame is being laid upon the good guys  – fat and cholesterol.  

Please click on and read our free peer reviewed medical journal publications and ask your medical advisors some tough questions about this low cholesterol ‘madness’.

“Cholesterol Lowering Therapies and Membrane Cholesterol”

Wainwright G   Mascitelli L  &  Goldstein M R

Archives of Medical Science Vol. 5 Issue 3 p289-295 2009

“Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?”

 Seneff S, Wainwright G, and Mascitelli L

Archives of Medical Science  Vol. 7 Issue 1 p8-20 2011 doi: 10.5114/aoms.2011.20598

“Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet”

Seneff S., Wainwright G., and Mascitelli L.

European Journal of Internal Medicine 2011  doi:10.1016/j.ejim.2010.12.0172011

Low Cholesterol – Madness

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Our letter to the Academy of Medical Royal Colleges Obesity Steering Group was acknowledged in Appendix B under the name of lead author Barry Groves (Second Opinions).

Clearly our message was diluted in the final report by other issues but you can read it here.

Obesity Is an Iatrogenic Disease
The Obesity Steering Group requested suggestions for action to halt the seemingly inexorable rise in obesity and associated conditions.

Action required
The only action which we feel needs to be taken is the dissemination of evidence-based, dietary advice by authorities. This will mean a complete reversal of the current disastrous ‘healthy eating’ experiment. We need to return to our natural diet.

Introduction
Being overweight has affected a small proportion of the population for centuries but clinical obesity was rare until the 20th century. It remained at a fairly stable low level until about 1980. The COMA report of 1984 advised us to eat a diet based on breads, pasta, fruit and vegetables, and low in fat, since when the incidence of obesity has increased dramatically. By 1992 one in every ten people in Britain was overweight. It is now more than one in four among adults. They didn’t become fat in the past 30 years because they became gluttonous and lazy, but because they got bad advice to eat carbohydrates. That is why obesity is iatrogenic, from bad nutritional (medical) advice.

‘Healthy eating’ is fattening
We have known for at least 150 years that obesity is caused solely by dietary carbohydrates – starches and sugars; and that reducing carbohydrate intake has a salutary effect.[1] It has also been demonstrated that increasing fat intake is slimming. These two facts, together with epidemiological studies and controlled clinical studies over some 80 years, which have confirmed a causal link, show clearly that ‘healthy eating’ could be expected to increase the incidence of obesity. Despite this evidence, carbohydrate-based, low-fat diets for the amelioration of obesity are promoted strongly by authorities who are clearly ignorant of this evidence and, thus, are not competent to give dietary advice.
More people are cutting calories and saturated fats now than ever before in their history yet more of them are becoming overweight. It may be hard to believe, but this has occurred in the face of increasing awareness and education about obesity, nutrition and exercise. It has happened despite the fact that calorie intake has gone down over the period and exercise clubs have mushroomed. There is now a pandemic of increasing weight across the industrialised world.
But it need not have happened, for 150 years ago one man changed thinking on diet completely.
It started with a small booklet entitled Letter on Corpulence Addressed to the Public, not written by a dietician or a doctor, but by an undertaker named William Banting. First published in 1863, it went into many editions and continued to be published long after the author’s death. The book was revolutionary and it should have changed western medical thinking on diet for weight loss forever.
William Banting began to get fat in his 30s. It was a condition he had always dreaded. Over the next thirty years, Banting tried every treatment the medical profession could offer. Nothing worked; he got fatter.

Treatments
One eminent surgeon recommended “increased bodily exertion before any ordinary daily labours began”. Banting had a heavy boat and lived near the river; he took up rowing for two hours a day. All this did for him, however, was to give him a prodigious appetite. He put on weight and was advised to stop! So much for exercise!
He was advised that he could remedy his obesity by “moderate and light food”. This brought his system into a “low, impoverished state without reducing [his] weight, which caused many obnoxious boils to appear and two rather formidable carbuncles”. He went into hospital and was ably operated upon – but also fed into increased obesity.
Banting went into hospital twenty times in twenty years for weight reduction. He tried swimming, walking, riding and taking the sea air. He drank “gallons of physic and liquor potassae”, took the spa waters at Leamington, Cheltenham and Harrogate, and tried low-calorie, starvation diets; he took Turkish baths at a rate of up to three a week for a year but lost only six pounds in that time, and had less and less energy.
He was assured by one physician that putting weight on was perfectly natural; that he, himself, had put on a pound for every year of manhood.
Banting tried every form of slimming treatment the medical profession could devise but it was all in vain. Eventually, discouraged and disillusioned – and still very fat – he gave up. By 1862, at the age of 66, Banting weighed 202 lbs and he was only 5 ft 5 ins tall. He also suffered many other chronic conditions.
Among these, his sight was failing and he was becoming increasingly deaf. Because of this last problem, in August 1862, Banting consulted Dr. William Harvey, FRCS. It was an historic meeting. When Harvey met Banting, he was interested as much by Banting’s obesity as by his deafness, for he recognised that the one could be related to the other. So Harvey put Banting on a diet.

Harvey’s anti-obesity diet
For each meal, Harvey allowed Banting:
• Up to six ounces of bacon, beef, mutton, venison, kidneys, fish or any form of poultry or game;
• The ‘fruit of any pudding’ – he was denied the pastry
• Any vegetable except potato;
• Tea without milk or sugar
• At dinner, two or three glasses of good claret, sherry or Madeira.
• Champagne, port and beer were forbidden and he could eat only one ounce of toast.
On this diet Banting lost nearly 1 lb per week from August 1862 to August 1863. In his own words he said:
“I can confidently state that quantity of diet may safely be left to the natural appetite; and that it is quality only which is essential to abate and cure corpulence… . These important desiderata have been attained by the most easy and comfortable means.”
After 38 weeks, Banting felt better than he had for the past 20 years. By the end of the year, not only had his hearing been restored, he had much more vitality and he had lost 46 lbs in weight and 12 ¼ inches off his waist.
Banting said of his diet:
“I can conscientiously assert I never lived so well as under the new plan of dietary, which I should have formerly thought a dangerous, extravagant trespass upon health.”
He says that this present dietary table is far superior to what he was eating before:
“more luxurious and liberal, independent of its blessed effect, but when it is proved to be more healthful, the comparisons are simply ridiculous.”
“I am very much better both bodily and mentally and pleased to believe that I hold the reins of health and comfort in my own hands.”
“It is simply miraculous and I am thankful to Almighty Providence for directing me through an extraordinary chance to the care of a man who worked such a change in so short a time.”
It is quite obvious from these comments that Banting didn’t need the strength of willpower that today’s slimmer needs; that he found his weight-loss diet very easy to maintain.
In the 1890s, American doctor, Emmet Densmore, modelled diets on Banting.[2] He tells how he and his patients lost an average 10-15 lbs in the first month and 6-8 lbs in subsequent months “by a diet from which bread, cereals and starchy food were excluded”. His advice to would-be slimmers was: “One pound of beef or mutton or fish per day with a moderate amount of the non-starchy vegetables [tomatoes, lettuce, string beans, spinach and such] will be found ample for any obese person of sedentary habits”.
In 1906, Dr Vilhjalmur Stefansson, revolutionised polar exploration by crossing the Arctic alone and living off the land with the Eskimos. It was a golden opportunity to conduct an experiment into the effects of an Eskimo diet on a European unaccustomed to it. On this regime, Stefansson remained in perfect health and did not get fat. It was evident to Stefansson, as it had been to Banting, that the body could function perfectly well, remain healthy, vigorous and slender on a diet in which as much food was eaten as the body required, only carbohydrate was restricted and the total number of calories was ignored.[3]

The first clinical dietary trial
In 1928, Stefansson and colleague, Karsten Andersen, entered Bellevue Hospital, New York, for a controlled experiment into the effects of an all-meat diet on the body.[4] The committee assembled to supervise the experiment was one of the best qualified in medical history, consisting as it did of the leaders of all the branches of science related to the subject. Dr. Eugene F. DuBois, Medical Director of the Russell Sage Foundation (subsequently chief physician at the New York Hospital, and Professor of Physiology at Cornell University Medical College) directed the experiment. The study was designed to find the answers to five questions about which there was some debate:
1. Does the withholding of vegetable foods cause scurvy?
2. Will an all-meat diet cause other deficiency diseases?
3. Will it cause mineral deficiencies, of calcium in particular?
4. Will it have a harmful effect on the heart, blood vessels or kidneys?
5. Will it promote the growth of harmful bacteria in the gut?
The results, published in the Journal of Biological Chemistry showed that the answer to all of the questions was: No. There were no deficiency problems; the two men remained perfectly healthy; their bowels remained normal, except that their stools were smaller and did not smell. The absence of carbohydrates from their diet appeared to have only good effects. Only when fats were restricted did they suffer any problems. Intakes varied between 2,000 and 3,100 kilocalories per day and averaged 80% of energy from animal fat and the other 20% from protein.

The evidence mounts
In 1932, a clinical study carried out at the Royal Infirmary, Edinburgh studied the effects of low- and high-calorie diets, ranging from 800 to 2,700 kcals, and with different macronutrient combinations.[5]
On 1,000 kcal isocaloric diets, average daily losses were:
• High carbohydrate/low fat diet – 49g
• High carbohydrate /low protein – 122g
• Low carbohydrate /high protein – 183g
• Low carbohydrate/high fat – 205g
Drs Lyon and Dunlop pointed out that:
“The most striking feature of the table is that the losses appear to be inversely proportionate to the carbohydrate content of the food. Where the carbohydrate intake is low the rate of loss in weight is greater and conversely.”
In 1953 Dr Albert Pennington also found that:
“weight loss appeared to be inversely related to the amount of glycogenic materials in the diet. Carbohydrate is 100%, protein 58% and fat 10% glycogenic.”
“The recommended diet is a calorically unrestricted one, very low in carbohydrate, high in fat and moderate in protein. Neither fat nor protein is restricted, however.” [6]
Pennington told his readers: “Most of the meat you buy is not fat enough, so get extra beef kidney fat, slice and fry it to make up the proper proportion.”
In 1956, Professor Alan Kekwick and Dr Gaston Pawan had similar results to Lyon and Dunlop. In a trial at the Middlesex Hospital, London, overweight patients:
• Lost the most weight on a high-fat, low-carbohydrate diet
• Lost the least weight on a carbohydrate-based, low-fat diet
• Lost weight even at 2,600 calories a day – but only on a high-fat diet.[7]
In 1959, Professor John Yudkin, Queen Elizabeth Hospital, University of London, confirmed Kekwick and Pawan’s findings when he showed that a diet with unlimited protein and fat, but with little or no carbohydrate was far more effective in causing weight loss than a calorie-controlled, low-fat diet.[8]
And there have been many more controlled studies this century.

Obesity is an iatrogenic disease
In 1994, Professor Susan Wooley and Dr David Gardner highlighted the role of the professional in people’s increasing weight, saying:
“The failure of fat people to achieve a goal they seem to want – and to want above all else – must now be admitted for what it is: a failure not of those people but of the methods of treatment that are used.
“We should stop offering ineffective treatments aimed at weight loss. Researchers who think they have invented a better mousetrap should test it in controlled research before setting out their bait for the entire population. Only by admitting that our treatments do not work – and showing that we mean it by refraining from offering them – can we begin to undo a century of recruiting fat people for failure.”[9]
But there is a ‘better mousetrap’. William Banting wrote of it 150 years ago.

All mammals naturally eat a high-fat diet
All herbivores, using microfloral activity, ferment large quantities of vegetable fibre and other carbohydrates to produce short-chain fatty acids which are absorbed for energy. Little or no carbohydrate is absorbed as glucose. Similarly, all carnivores eat and absorb saturated animal fats, and no carbohydrates. In fact, whether herbivore, omnivore or carnivore, the natural diet of all mammals is high in total fats and saturated fats and low in carbohydrates. In nature, no animal is overweight and none suffers the chronic degenerative diseases we ‘civilised’ humans do. This also applies to ‘primitive’ human cultures.
Our natural diet is a high-fat diet, just like every other mammal.[10] We disregard this fact at our peril.
And saturated fat is best
Scientists at the Faculty of Medicine, University of Geneva, found that the more saturated a fat was, the less likely it was to increase a person’s weight.[11] This is not surprising as saturated fats are lower in calories than unsaturated fats.[12, 13]

Conclusion
Current ‘wisdom’ champions high-carbohydrate, low-fat diets as optimum, while dismissing higher protein/fat, low-carbohydrate diets as dangerous. Yet the evidence from evolutionary, epidemiological and clinical trials shows conclusively that the healthiest diet for weight loss (and many other diseases) is the exact opposite: one which is high in animal fats and protein, low in carbohydrates, particularly from cereals, legumes and fruit, and where calories are unrestricted. It is no coincidence that the incidence of obesity has risen so dramatically since ‘healthy eating’ was introduced – it’s a classic example of cause and effect.
Yet, despite the overwhelming weight of evidence that ‘healthy eating’ is not healthy, unsupported dogma still rules as leaders in medicine continue to ignore science and even their own experience, and push a grotesque diet which has led to today’s gross obesity and runaway diabetes.
Let us leave the last word to Dr Sylvan Lee Weinberg, past president of the American College of Cardiology and previously a fervent supporter of ‘healthy eating’. In 2004, Weinberg wrote in the Journal of the American College of Cardiology:
“The low-fat, high-carbohydrate diet … can no longer be defended … by rejecting clinical experience and a growing medical literature suggesting that the much-maligned low-carbohydrate, high-protein diet may have a salutary effect on the epidemics in question.”[14]
Like every other mammal on Earth, we should eat a high-saturated fat, low-carbohydrate diet.

Signatories
Barry Groves, PhD. Independent nutritional researcher and author. Oxford, UK.
Dr David Brownstein, MD, Medical Director, Center for Holistic Medicine, Michigan
Dr Robert Davidson, MD PhD. Fellow, American Institute of Stress, Internal Medicine Doctor, Texas
Marshall E. Deutsch, PhD (Physiological Sciences) Independent investigator. Sudbury, Massachusetts.
Professor David Diamond, PhD, Professor, Departments of Psychology, Molecular Pharmacology and Physiology; Research Career Scientist, Medical Research Service, Veterans Hospital, Tampa, FL, USA
Dr Duane Graveline, MD MPH. former NASA Astronaut, USAF Flight Surgeon, Space Medicine Research Scientist, Family Doctor, Florida.
Professor M Canan Efendigil Karatay, Cardiologist and İnternist, İstanbul Science University Medical Department.
Dr Malcolm Kendrick, MbChB, MRCGP (exam). General practitioner in Macclesfield.
Dr Peter Langsjoen, MD, FACC, Cardiologist and Internist, private practice, Tyler, Texas.
Lt Col. Dr Luca Mascitelli, MD, Medical Service, Comando Brigata Alpina “Julia”, Udine, Italy
Carlos Monteiro, President, Infarct Combat Project.
Dr Uffe Ravnskov, MD, PhD, specialist in internal medicine and nephrology, independent researcher, Lund, Sweden
Professor Paul J. Rosch, MD, FACP. President The American Institute of Stress; Clinical Professor of Medicine and Psychiatry, New York Medical College; Honorary Vice President, International Stress Management Association
Dr Stephanie Seneff, Senior Research Scientist, MIT, Cambridge, Massachusetts.
Glyn Wainwright, MSc, MBCS, CEng, CITP. Independent Reader of Research, Leeds, UK

Correspondence to barrygroves@tiscali.co.uk

References
1. William Banting. Letter on Corpulence, 1863.
2. Emmet Densmore. How Nature Cures. 1892.
3. Vilhjalmur Stefansson. The Fat of the Land. 1946.
4. McClelland WS, du Bois EF. Clinical Calorimetry. XLV, XLVI, XLVII Prolonged meat diets with a study of kidney function and ketosis. J Biol Chem 1930-1931; 87: 651-658; 87: 669; and 93: 419.
5. Lyon DM, Dunlop DM. The treatment of obesity: a comparison of the effects of diet and of thyroid extract. Quart J Med 1932;1:331-52.
6. Pennington AW. A Reorientation on Obesity. New Eng J Med 1953;248: 959-64.
7. Kekwick A, Pawan GLS. Calorie intake in relation to body-weight changes in the obese. Lancet 1956; ii: 155-160.
8. Yudkin J. The Causes and Cure of Obesity. Lancet 1959;II(7112):1135-8.
9. Wooley SC, Garner DM. Dietary treatments for obesity are ineffective. BMJ 1994; 309: 655-6.
10. Ben-Dor M, et al. PLoS ONE 2011; 6(12): e28689.
11. Dulloo AG, et al. Metabolism 1995; 44: 273-279.
12. Lars A Carlson; Sven Lindstedt. The Stockholm prospective study. 1: The initial values for plasma lipids Almqvist & Wiksell, Stockholm, 1968.
13. Apgar JL, Shively CA, Tarka SM. Digestibility of cocoa butter and corn oil and their influence on fatty acid distribution in rats. J Nutr 1987;117: 660-665
14. Weinberg SL. The Diet-Heart Hypothesis: a Critique. J Am Coll Cardiol 2004;43:731–733.

Further reading
Volek JS, Feinman RD. Carbohydrate restriction improves the features of metabolic syndrome. Metabolic syndrome may be defined by the response to carbohydrate restriction. Nutr Metabol 2005;2:3148.
Westman EC, Yancy WS, Haub MD, Volek JS. Insulin resistance from low carbohydrate, high fat diet perspective. Metabol Syndr Relat Dis 2005;3:14-18.
Cannon MC, Nuttall FQ. Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutr Metabol 2006;3:16-23.

Letter on Obesity to the Academy of Medical Royal Colleges

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Fructose Has Different Effect Than Glucose On Brain Regions That Regulate Appetite

Jan. 1, 2013 — In a study examining possible factors regarding the associations between fructose consumption and weight gain, brain magnetic resonance imaging of study participants indicated that ingestion of glucose but not fructose reduced cerebral blood flow and activity in brain regions that regulate appetite, and ingestion of glucose but not fructose produced increased ratings of satiety and fullness, according to a preliminary study published in the January 2 issue of JAMA.

JAMA and Archives Journals (2013, January 1). Fructose has different effect than glucose on brain regions that regulate appetite.

Fructose Has Different Effect Than Glucose On Brain Regions That Regulate Appetite

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Effects of Fructose vs Glucose on Regional Cerebral Blood Flow in Brain Regions Involved With Appetite and Reward Pathways

Kathleen A. Page, MD; Owen Chan, PhD; Jagriti Arora, MS; Renata Belfort-DeAguiar, MD, PhD; James Dzuira, PhD; Brian Roehmholdt, MD, PhD; Gary W. Cline, PhD; Sarita Naik, MD; Rajita Sinha, PhD; R. Todd Constable, PhD; Robert S. Sherwin, MD
JAMA. 2013;309(1):63-70. doi:10.1001/jama.2012.116975

Importance  Increases in fructose consumption have paralleled the increasing prevalence of obesity, and high-fructose diets are thought to promote weight gain and insulin resistance. Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion, and central administration of fructose provokes feeding in rodents, whereas centrally administered glucose promotes satiety.

Objective  To study neurophysiological factors that might underlie associations between fructose consumption and weight gain.

Design, Setting, and Participants  Twenty healthy adult volunteers underwent 2 magnetic resonance imaging sessions at Yale University in conjunction with fructose or glucose drink ingestion in a blinded, random-order, crossover design.

Main Outcome Measures  Relative changes in hypothalamic regional cerebral blood flow (CBF) after glucose or fructose ingestion. Secondary outcomes included whole-brain analyses to explore regional CBF changes, functional connectivity analysis to investigate correlations between the hypothalamus and other brain region responses, and hormone responses to fructose and glucose ingestion.

Results  There was a significantly greater reduction in hypothalamic CBF after glucose vs fructose ingestion (−5.45 vs 2.84 mL/g per minute, respectively; mean difference, 8.3 mL/g per minute [95% CI of mean difference, 1.87-14.70]; P = .01). Glucose ingestion (compared with baseline) increased functional connectivity between the hypothalamus and the thalamus and striatum. Fructose increased connectivity between the hypothalamus and thalamus but not the striatum. Regional CBF within the hypothalamus, thalamus, insula, anterior cingulate, and striatum (appetite and reward regions) was reduced after glucose ingestion compared with baseline (P < .05 significance threshold, family-wise error [FWE] whole-brain corrected). In contrast, fructose reduced regional CBF in the thalamus, hippocampus, posterior cingulate cortex, fusiform, and visual cortex (P < .05 significance threshold, FWE whole-brain corrected). In whole-brain voxel-level analyses, there were no significant differences between direct comparisons of fructose vs glucose sessions following correction for multiple comparisons. Fructose vs glucose ingestion resulted in lower peak levels of serum glucose (mean difference, 41.0 mg/dL [95% CI, 27.7-54.5]; P < .001), insulin (mean difference, 49.6 μU/mL [95% CI, 38.2-61.1]; P < .001), and glucagon-like polypeptide 1 (mean difference, 2.1 pmol/L [95% CI, 0.9-3.2]; P = .01).

Conclusion and Relevance  In a series of exploratory analyses, consumption of fructose compared with glucose resulted in a distinct pattern of regional CBF and a smaller increase in systemic glucose, insulin, and glucagon-like polypeptide 1 levels.

Fructose & Obesity – JAMA Report

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Fighting the flab means fighting makers of fatty foods -WRONG !!!  – New Scientist Opinion Column

My response to this article in New Scientist this week:-

Carbohydrates and insulin are obesogenic and dietary fats are not obesogenic.

The Danish politicians who taxed fat were the victims of erroneous medical advice.

Sugar causes obesity, and we explain further in our research review paper:

Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?

Seneff S, Wainwright G, Mascitelli L.

Arch Med Sci. 2011 Feb;7(1):8-20 Epub 2011 Mar 8.

doi: 10.5114/aoms.2011.20598

PMCID: PMC3258689

Dietary Fats are not Obesogenic – Sugar does it!