Are there any studies of sugar consumption, natural or randomized that support this, or are you asking for such studies?

I agree completely. Because of the sugar added to most prepared foods, our metabolism cannot get to a fat metabolism. Eating sugar lends to hypoglycemia and craving for more sugar. Our pancreas is not used to so much sugar, nor are the microbes in the gut. The body tries to normalize high insulin by dumping it into fat cells or creating an insulin attacting tumor in places like the prostate. Sugar addiction is one of the curses of the modern world, used by companies to encourage the addiction.

The Canadian sugar consumption is 110.0 grams /day and amounts to 21.4% of total caloric intake. ( Health Reports Canada vol.22,no.3,Sept 2011. It is very likely that promotion of low-fat diet and replacing calories with refined carbohydrates contributed to North American obesity epidemic.

I think you hit on some very key points Richard, those being that when we talk about weight management it isn't simply retsricting calories, it is structuring our food plans to take into account the time we eat, the portions, the number of meals per day, and most importantly-the kinds of food we take in i.e. refined sugars, types of fat etc. However, without involvement from the food, FDA and advertising industries it will be difficult to achieve sustainable results. When you mention paradigm shifts, it will take involvement from both the individual and business/governement policy levels. We can already see from the state level where municipalities are banning sugary drinks (New York) in certain areas--reminds me of the smoking bans that slowly crept into existance stemming from both municipal and employer level policy making. I recently read a comment from a physician who is recognized as a national expert on metabolic syndromes and diabesity whereby he stated that if every man , woman and child in the US were to cut back 100 calories a day from their daily energy intake--the food industry would stand to lose anywhere from 30-40 billion dollars per year. So are the food manufacturer's likely to be partners in this entire initiative of lowering food portions, reducing consumption of red meats, sugars, and processed foods in general-probably not willing partners at first.

That's actually a valid point, though. In the US, sugar is ubiquitous. It's in everything from peanut butter to salad dressings. One of my colleagues once commented that she didn't like our bread (the commercial stuff) because it was too sweet. I don't understand why we need sugar in peanut butter (or salad dressing) or a myriad of other things--and trying to limit our intake is very difficult because its use is so widespread. The only good way around it in the US is to eat nothing that it pre-packaged, and that's not entirely foolproof--some of our citrus fruits and other foods are injected to make them sweeter! Artificial sweeteners aren't a help in this--the statistics indicate that consumption of diet sodas is highest among the obese population, and numerous studies implicate them in aberrant satiety hormonal signaling. However, it is still inaccurate to blame sugar entirely for the issue, as portion control and lack of physical activity are also major contributors.

The postprandial metabolism of fat and sugar are different. Higher fat intake is accompanied by feeling of satiety, high sugar intake is frequently followed by mild hypoglycemia and urge to look for a snack.

What is "sugar"? Are you referring to the white, granular material that is sucrose, a disaccharide composed of glucose and fructose? Certainly an over-consumption of sucrose plus a variety of sweeteners with different configurations of the same glucose and fructose components are contributing to our growing levels of obesity and non-communicable chronic diseases. In the popular press, which includes prominent internet sites, both sucrose and maybe high fructose corn syrup have been fingered as the sole contributors to the obesity epidemic. So too has an over-consumption of the high carbohydrate foods that humans digest rapidly; these are commonly called high glycemic index foods.

Instead, could it be the paucity of soluble and insoluble fibers in the typical modern diet that are driving the health crisis? People who consume a diet with a preponderance of simple carbohydrates tend to ingest low levels of either form of fiber. Or could the health issues be due to trans fats, particularly the artificial ones that are created to lengthen the shelf life of prepared foods? Clearly, research has shown a strong link to trans fats.

And what about abundant sedentary behaviour that we now demonstrate, driven by increased screen time? And the typical aversion to vigorous physical activity that affects most people, often after the age of about 12, let alone 50? Research has clearly shown that any movement is healthier than none and vigorous work performed by large skeletal muscles both upregulates insulin sensitivity and selectively decreases central adiposity.

Fingering "sugar" intake as the sole contributor the health or obesity crisis is overly simplistic. Yes, we know it hurts us, as do some other dietary components. We also suffer from a lack of what we are not getting in sufficient doses, namely foods with health benefits and vigorous physical activity.

The huge question is really how are we going to fix the health problems that are driven by poor diets and insufficient physical activity. Telling people that they should not eat something or should eat something else has poor efficacy, as does telling people to move more. So how do we tackle this? What are likely the most important factors that lead to longterm improvements in healthy behaviour? And what are some excellent research studies that we can conduct?

Richard - I am interested in your comment that meta-analyses show fat as being part of the solution, not part of the problem. Do you have any references you can cite so I can check these out? I think heavy doses of fat in foods leads to overeating. David Kessler's (former FDA chief) book "the end of overeating" is great and goes into detail about why fat leads to overeating. Actually, it's the combination of fat and sugar in particular, though combinations of either with salt also is a factor.

Jo, I agree with most of your comments. Unfortunately most trials studying methods of weight reduction work in short term; within a year the respondents usually regain i their original weight. And you are also right that the issue is not only caloric intake; future trials should explore the possibilities of changing health behavior.

In answer to which sugars, it is glucose and fructose and they as act on independent pathways the pathophysiologic effects are a complex of both. The consumption of other specific sugars probably have not reached the pharmacologic effect levels of glucose and fructose.

References for lack of adverse effects of fat consumption (excluding trans fats which are a different issue) Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition. 2010 Mar. 1;91(3):535–46. HITE AH et al In the face of contradictory evidence: Report of the Dietary Guidelines for Americans Committee. Nutrition. 2010 Oct. 1;26(10):915–24. Hite AH, Berkowitz VG, Berkowitz K. Low-Carbohydrate Diet Review: Shifting the Paradigm. Nutrition in Clinical Practice. 2011 May 16;26(3):300–8. Volek J, Fernandez M, Feinman R, Phinney S. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Progress in Lipid Research. 2008 Sep. 1;47(5):307–18. Also of note, the Women's Health Initiative Study dietary intervention (low fat) was negative for mortality reduction.

In children specifically, exercise does not reduce obesity. Might want to see Bremer AA, Mietus-Snyder M, Lustig RH. Toward a Unifying Hypothesis of Metabolic Syndrome. PEDIATRICS. 2012 Mar. 1;129(3):557–70.

The exercise issue is one of calorie in-calorie out without any consideration of the physiologic control mechanisms controlling hunger and exercise. Very low sugar diets try to reset these mechanisms. maybe why non-calorie restricted very low carb diets are successful. The key is no calorie restricted so it is the normal physiologic control mechanisms that are being accessed that result in the reversal of the metabolic syndrome manifestations

High sugar consumption is not the only factor but a contributing factor. Excess circulating sugar can be a problem. Other attendant factors are artificial sweeteners, esposure to chemicals, eg mosquito repellents, perfumes (as they contain aluminium compounds), and drug consumption as there can be drug-induced diabetes. A lot of research points to central obesity as a contributing factor as adipocytes release inflammatory factors that can can suppress beta-cell activity.

Several studies estimate that 30-50% of the world's population has some degree of microparsasite (protozoal ) infection and their infective forms (tachyzoites and sporozoites) can disturb ion (Ca2+) chanelling thereby increasing oxidative stress and immune suppression mediated through inflammatory factors and induction of glycosylation etc. They can trigger abnormal activation of NFkappaB with Ca2+ or TNF that can lead to formation of abnormal proteins etc and can become another factor in immune suppression. Protozoa also utilize vitamin B12 for their protein synthesis depleting it in about 25-35% of people who may have some form of vitamin B12 deficiency. Vitamin B12 is an important regulatory molecules that is involved in many pathways, including the B12-haptocorin conjugation and in the synthesis of dopamine serotonin etc. A defiency in vitamin B12 increases risk to cancers. This vitamin B12 link relates to depression in some obese peole

A shift away from the "primate diet pattern" consisting of raw fruits (and salads) to nourish the body with a broad range of natural antioxidants towards "fast foods" is rather tragic that also contributes to a redox imbalance. Once hyperglycemia is induced and if the redox balance is not corrected through clinical nutrition, it can progress into several complications.

Alloan-induced diabetic rat studies indicate that calalase and SOD enzyme levels decline in tissues and organs, including in the heart. Since this enzyme system converts OFR into water and oxygen, a decline in its acitivity will lead to increassing ROS levels followed by the formation of secondary raicals, like the hydroxyl radical, leading chronic disease states. Fortunately, there are herbal formulations that can treat such problems with consequent increase in catalase-SOD levels, something that cannot be achieved with drugs as drugs generate free radficals in biological systems. I will register a patent on one such formulation soon.

Inflammation in the body (such as that maintained by protozoa) or drugs can also disturb the leptin-ghrelin balance that alters satiety and hunger biochemical mechanism. Obesity, diabetes and cancers have a common underlying link - inflammation and can be viewed as systemic inflammatory disease.

The many views above are appreciated and valid. Taking small amounts of raw sugar to replace white sugar is certainly a good idea because raw sugar has some anti-inflammatory effects.Excess alcohol together with excess white sugar intake and too many carbonated drinks is not a good combination as it can disturb healthy biochemistry. Chromium deficiency can also be a problem in a small group pf people as it conjugates with insulin for binding on to receptors on cells wherein such binding allows glusose to enter cells. It is a complex biochemistry and diabetes is a multifctorial problem related to redox imbalance and altered biochemistry. It cannot be fully explained or dealth with in a brief manner such as in this column. Regards.

Throughout the 20th Century, sugar and omega-6 industrial seed oil consumption increased concurrently. Interestingly, it wasn't until around 2004 that sugar got any bad press(1). At that point per capita consumption had climbed way beyond what might be considered prudent. Omega-6 seed oils(2) are still pretty much in the background as the vast majority of health experts have been trained to believe that saturated fat is the major food component responsible for heart disease(3). The diet heart hypothesis coupled with the idea that high fat intake promotes weight gain has caused considerable mischief(4). It's time consumers were warned about omega-6 industrial seed oils(5) and reassured about the benefits of saturated fat(6,7,8).

References

1. http://www.ajcn.org/content/79/4/537.full

2. http://www.psychologytoday.com/blog/evolutionary-psychiatry/201103/your-brain-omega-3

3. http://www.omen.com/corr.html

4. http://jhmas.oxfordjournals.org/content/63/2/139.full

5. http://sciencenordic.com/vegetable-oils-promote-obesity

6. http://www.meandmydiabetes.com/2012/04/17/ron-krauss-saturated-fat-red-meat-it-depends/

7. http://www.youtube.com/watch?v=vRe9z32NZHY

8. http://healthydietsandscience.blogspot.com/search/label/Saturated%20Fat%20and%20Heart%20Disease

The representative EsKiMo-Study (part of KiGGS-Study = Child and Adolescence Health Survey in Germany, 2007) shows, that 6 year old boys are consuming 5kg sugar/year via Lemonade only (Sugar, aroma, water) and this amount gradually grows until 30kg/year in the age of 15-17.

Stahl, A., C. Vohmann, A. Richter, H. Heseker and G. B. Mensink (2009). "Changes in food and nutrient intake of 6- to 17-year-old Germans between the 1980s and 2006." Public Health Nutr: 1-12.

This may be one reason why obesity in children and adolescsents rose lately in Germany (and there are no signs of a reversed trend until today).

Rosario, A. S., B. M. Kurth, et al. (2010). "Body mass index percentiles for children and adolescents in Germany based on a nationally representative sample (KiGGS 2003-2006)." Eur J Clin Nutr 64(4): 341-9.

The evidence base for a causal correlation of sugar consumption and obesity in children is considered as "probable" by the German Society of Nutrition (Grade 2 of 4).

Do we really have to wait for evidence based knowledge in the last details when rising obesity rates and rates of noncommunicable diseases are already threatening the achievement of the UN Millennium Goals in low and middle income countries and are driving health systems and economies of industrialized countries to the edge(which are under stress anyway)? Societies have to act now to prevent more harm. In September 2011 the first UN-Summit on Prevention and Control of Noncommunicable Diseases (NCDs) took place in New York. The United Nations unanimously adopted a political declaration and in May 2012 the WHO adopted the overarching target to reduce NCDs by 25% until 2025. The four main risk factors were named: unhealthy food (!), lack of physical activity, harmful use of alcohol and tobacco.

diabetesDE - German Diabetes Aid started a petition, named: “No sugary drinks at school!” that is running until the end of July 2012. The German Obesity Association (www.adipositas-gesellschaft.de) is our partner in this project. In Germany the 16 Länder (regions) are responsible for the schools, so we want to start this project in Berlin as a good practice model for the other Länder.

For the beginning of the new school term in the middle of August we are planning a public handing over of the signatures to a prominent German politician. This will take place at a good practice school in Berlin running a drinking water well for pupils and teachers.

If you want to support this initiative, would be very grateful if you would sign and/or help to spread our petition (which unfortunately is in German):

http://www.petitiononline.de/petition/schulfrei-fuer-zuckerhaltige-getraenke/887

The UN-Summit on Prevention and Control of Noncommunicable Diseases made at least three major mistakes. It targeted saturated fats(1), recommended fat restriction to lose weight(2), and ignored the omega-6 hazard(3). Quote(4):

Total Fat – limit total fat to 15-30% of energy intake.

Trans Fat – total elimination from the food supply by 2020.Saturated Fat – limit saturated fat intake to less than 10% of energy intake.

References

1. http://www.omen.com/corr.html

2. http://jhmas.oxfordjournals.org/content/63/2/139.full

3. http://www.foodproductdesign.com/articles/2012/06/new-generation-of-fried-foods.aspx

4. http://www.wcrf.org/cancer_research/policy_advocacy/un_summit.php

The sugar over consumption wear out the pancreatic cells more quickly. If the over consumption of lipids also occurs, deterioration is worse. If we also have lack of exercise the problem is unavoidable.

Restricting sugar intake will not make the obese thin. Unfortunately, some metabolic changes may be nearly irreversible. Fortunately, health benefits will result from replacing sugar with fiber and whole foods, independent of weight loss.

The Diabetes Prevention Trial, for example, is often cited as proof that tiny weight losses can translate into big health benefits. But the intervention was nothing short of a lifestyle makeover, with several fold increase in weekly exercise, and decreased intake of sugar and saturated fat. These major lifestyle changes, not the minor loss of body weight, are what drove the health benefits.

Our greatest problem is measurement of factors contributing to obesity. That said, even our crude measures still are suggestive that our intake of sugar-based products, particular soft/soda drinks are associated with increased adiposity. (eg Rissel CE, Reinten-Reynolds TA, Wen LM, Hardy LL. Soft drink consumption and obesity in NSW school students. Med J Aust 2012; 196(3):171-172.)

While the latest NYC intervention by Bloomburg to limit the the volume of soft drinks is couched in 'nanny-state' politics, it potentially is efficacious - folk who think that ordering 2 lites of soft drink (ie 63 gms of sugar) is 'normal' need public policy interventions. Awarness raising is not working.

Quoting Paul Ernsberger: "But the intervention was nothing short of a lifestyle makeover, with several fold increase in weekly exercise, and decreased intake of sugar and saturated fat. These major lifestyle changes, not the minor loss of body weight, are what drove the health benefits."

The decrease in saturated fat probably had a negative effect on both health and body fat composition. Saturated fats, especially the medium chain triglycerides, are very useful for weight control because they support testosterone production and thyroid function. And in the context of adequate supportive nutrition, saturated fats do not have an artery clogging effect, even at high intake levels.

http://www.meandmydiabetes.com/2012/04/17/ron-krauss-saturated-fat-red-meat-it-depends/

http://www.docsopinion.com/2012/06/04/the-case-against-saturated-fat/

http://www.health-report.co.uk/saturated_fats_health_benefits.htm

Lard sandwiches, anyone? On white or wheat bread? And would you like that bread fried? Certainly saturated fats are no panacea.

Mr. Bloomberg has the right idea, but regulation should be rather at the level of the food industry than the individual citizen. The present "environmental" doses of sugar & co. are toxic and, for example, just as damaging for the liver as alcohol. It should be treated similarly.

"Things should be made as simple as possible – but not simpler".

Obesity is a complex problem and I think high sugar as unique culprit is simplicity. High content on sugar or fat is just one point. I wonder what doesn't exist at processed food because there is a high content of sugar and fat.

The obesity epidemic is at least as complex as body weight regulation itself is. The question that has to be seriously addressed is, what can be changed, what are we stuck with? Or do we wait for self-regulation, since the life expectancy is now levelling off and maybe receding due to the obesity co-morbities.

Wow interesting

Dietary interventions that decrease caloric intake all work, while the individuals are compliant. The very low carbohydrate ketogenic VLCK diets are not calorie restricted, a very fundamental difference to almost all other interventions. Although not calorie restricted, they are as effective, or more so, as calorie restricted diets. The reduction in inflammatory markers in VLCK diets has been well documented. Does this improve long term compliance? Not yet known except through testimonial type evidence, not really sufficient for an evidence-based recommendation, but at least should lead to further studies.

It is critical in this discussion to separate causal elements from results. Studies in children clearly show exercise reduction is a result of obesity not a cause.

Arch Dis Child doi:10.1136/adc.2009.175927. Fatness leads to inactivity, but inactivity does not lead to fatness: a longitudinal study in children

There are many associations in studies but none withstand critical appraisal except that something happened in the 70's and since and the only causal association that fits all the data, is increased sugars consumption. I recommend, it you have access, looking at the BBC three part documentary series, Men Who Made Us Fat. The first two parts are well worth the effort of finding and watching. The third part is scheduled to be aired July 12.

The "Fatness leads to inactivity..." paper referenced by Richard Mathias is a very interesting study published in 2011 by Metcalf BS et al. 202 children, roughly equal numbers of boys and girls, 25% OW/obese, wore accelerometers once a year from age 7-10 and their body composition was measured by DXA. Thus, solid objective measures were employed in the study. While their results are enticing, one study that is not an intervention and entailed one cohort of children must be interpreted with caution.

A Cochrane review by Waters E et al ("Interventions for preventing obesity in children". Cochrane Database Syst Rev. 2011 Dec 7;(12):CD001871) examined 55 studies that tested a variety interventions for a total of about 30,000 children (ages 1-18, in 3 age brackets) and concluded that both dietary and physical activity interventions could be effective, especially with younger children. Few studies have been able to examine the longterm sustainability of interventions that targeted body composition. However, both the Cochrane review by Waters et al with the older group of children (13-18y) and other studies with adults, report that longterm compliance with dietary changes is poor.

My personal observation is that in some populations, various forms of simple sugar seem to be the source of excess caloric intake but in others, the culprit appears to be the serving sizes and number of servings of breads/pasta/rice. Indeed, in some Asians countries, white rice is currently fingered as the culprit in rising rates of diabetes. Others ingest excessive calories from fat (who needs to eat a "truck drivers' special" these days!!).

Thanks Jo but the Walters meta-analysis did not take sugars consumption into account so it is basically a review of observational studies which cannot do anything more than yield a hypothesis to be tested with much better control of confounding, i.e. randomization. I use the term sugars quite deliberately as it refers to simple sugars and also to foods where starches are quickly broken down into their constituent parts, hence rice, pasta, breads etc are part of the problem. The other component, of many sugars, fructose is also an issue with lipogenesis with the

production of very low density lipoproteins with high cardiovascular risk. I note the the compliance studies were not specifically calorie unrestricted. The basis of the low sugar diets (or very low carb ketogenic diets) is to stop the excess insulin stimulation caused by glucose and allow physiologic control process to return to normal function. I agree entirely that the advertising and availability issues requires more than individually based interventions but we can apply much of what we learned in tobacco control to sugars. Individual and public programs are quite compatible and each can strengthen the other but it requires that the paradigm shift from the behavioural and simplistic calorie in calorie out approach to one much more nuanced and physiologically based.

I think that the massive replacement of sugar in proteins are very bad for human nutrition.

Could you please explain what you mean, Ana Maria? I don't understand.

Sausage and luncheon with low cost are add with sugar (flour are cheaper, low cost), and good proteins (cow, etc) are replaced with soy proteins.

Consumption of glucose and the glycemic index/load of the diet do not produce insulin resistance or increase lipids (or produce inflammation). It is the fructose component of dietary sugars that does this . See these papers for detailed evidence:

Metabolic responses to prolonged consumption of glucose- and fructose-sweetened beverages are not associated with postprandial or 24-h glucose and insulin excursions. Stanhope KL, Griffen SC, Bremer AA, Vink RG, Schaefer EJ, Nakajima K, Schwarz JM, Beysen C, Berglund L, Keim NL, Havel PJ. Am J Clin Nutr. 2011 Jul;94(1):112-9. Epub 2011 May 25.

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. J Clin Invest. 2009 May;119(5):1322-34. doi: 10.1172/JCI37385. Epub 2009 Apr 20.

Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-B in young men and women. Stanhope KL, Bremer AA, Medici V, Nakajima K, Ito Y, Nakano T, Chen G, Fong TH, Lee V, Menorca RI, Keim NL, Havel PJ. J Clin Endocrinol Metab. 2011 Oct;96(10):E1596-605. Epub 2011 Aug 17.

Circulating concentrations of monocyte chemoattractant protein-1, plasminogen activator inhibitor-1, and soluble leukocyte adhesion molecule-1 in overweight/obese men and women consuming fructose- or glucose-sweetened beverages for 10 weeks. Cox CL, Stanhope KL, Schwarz JM, Graham JL, Hatcher B, Griffen SC, Bremer AA, Berglund L, McGahan JP, Keim NL, Havel PJ. J Clin Endocrinol Metab. 2011 Dec;96(12):E2034-8. Epub 2011 Sep 28.

Ana María Sánchez Peralta:

You mentioned that the overconsumption of sugar leads to worn out pancreas cells. I presume that this is because of continuously elevated levels of insulin? Just out of curiosity, would elevated levels of insulin also promote tumor growth, especially within the pancreas because the pancreas secretes insulin? That is, do you think one potential cause of pancreatic cancer, which is so difficult detect in early stages, may be sugar overconsumption?

Caleb Picker,

I'm studying the relationship between low functional insulin (resistance and low level of insulin) and the cancer. Insulin is a differentiation factor of cell, and the differentiation is the opposite of cancer. The high level of sugar on blood implies the wear of pancreatic cell, the resistance of insulin (no well effect on receptor) (insulin can be high to counter with this low effect) and finally with deficit of insulin. But I am looking for it now...

But cancer cell need more sugar because need more energy for quickly division. And insulin helps to this entrance of sugar. But all is regulated for different ways.

There is evidence that cancer cells require glucose and that removing glucose from them will kill the cancer cells. I have seen preliminary work in an animal model that increased survival with very low carbohydrate ketogenic diets. I have not seen similar studies in humans but it is an encouraging area for research. The reference below is again in a cell model system but is current and encouraging. Certainly fits with the concerns about excess glucose intake.

Glucose deprivation activates feedback loop that kills cancer cells: study June 26, 2012 in Cancer

In my publication is a reference, "It has been proved that to obtain mice which develop hepatocarcinogenesis induced by diethyl nitrosamine (DEN), the results are greater if diabetes is also induced in them by injecting streptozotocin (STZ) [18]."

[18] Saha BK, Sarkar A, Basak R, Chatterjee M. 1alpha, 25-Dihydroxyvitamin D3 suppresses the effect of streptozotocin-induced diabetes during chemical rat liver carcinogenesis. Cell Biol Int. 25 (3) (2001), pp. 227-37.

Diabetes helps to obtain cancer in rat.

Could there also be a genetic element involved? I.e. to explain, somewhat, why two individuals who consume the same amount of sugar and who are equally inactive increase weight at different rates.

I totally agree with Peter Havel's comments, fructose is the bad guy. The human body is really not set up to handle fructose well. The vast majority of fructose ingested is metabolized in the liver using up ATP and producing adenosine which in turn is converted to uric acid. There are no feedback controls on fructose metabolism as there are with glucose. Fructose is also metabolized in the kidney. The marked increase in liver and kidney disease can be correlated with the increase in fructose intake over the last 40 years.For a good read purchase Richard Johnson's book The Sugar Fix and if you would rather listen enter Lustig Fructose into google and get an excellent 80 minute lecture on fhe toxic effects of fructose which include hypertension, obesity, liver disease, kidney disease, type 2 diabetes.

With the more recent press about sugar (fructose) and its harmful effects, how long do you guys think until the FDA (or other governing bodies) will be able to save America (and the other parts of the world now on a Western diet) from the sugar pandemic?

For those of you who research this area, I sincerely thank you.

@ Caleb Picker

Unfortunately, neither government nor academia are equipped to furnish the public with an effective solution to the current epidemics of obesity, diabetes, and noncommunicable disease. Why? Because corporate interests have positioned themselves to control the content of dietetics education, and by extension, government policy. For example, the International Food Information Council Foundation(IFICF), financed by food and beverage interests, has close ties with academia, government, and the media. Here's what the IFICF says about itself:

"Incorporated as a public education foundation in 1991 and based in Washington, DC, the International Food Information Council Foundation is independent and not-for-profit. We do not lobby or further any political, partisan, or corporate interest. We bring together, work with, and provide information to consumers, health and nutrition officials, educators, government officials, and food, beverage, and agriculture industry professionals. We have established partnerships with a wide range of credible professional organizations, government agencies, and academic institutions to advance the public understanding of key issues. For example, we have a long-standing relationship with the U.S. Department of Agriculture Center for Nutrition Policy and Promotion as part of the Dietary Guidelines Alliance, a public-private partnership focused on the U.S. Dietary Guidelines for Americans and the MyPlate Food Guidance System. Recognizing the global nature of food safety, nutrition and health issues, the Foundation extends its mission internationally. We share education materials with an independent network of Food Information Organizations and partners from around the world. We also serve as a news media resource. We provide science-based information to the media and refer journalists to our 350 independent, credentialed experts on a variety of nutrition, food, and safety topics...We believe in the importance of educating health and nutrition professionals. We regularly host Continuing Professional Education (CPE) programs which are offered in person and via Web cast, and have developed a series of Commission on Dietetic Registration, the credentialing agency for the American Dietetic Association, CPE-approved learning modules on a variety of subjects."

http://www.foodinsight.org/about-ific-and-food-safety.aspx

For decades, the government's dietary advice has routinely favored the interests of the food manufacturing industry(1). Only recently have scientists begun to question the conventional wisdom regarding added sugars, saturated fats, and omega-6 industrial seed oils. Sadly, we're still being advised to replace saturated fats with omega-6s(2). Scientists concerned about the omega-6 hazard are few and far between(3).

The problem is consensus science. Scientific consensus is what the food manufacturing industry promotes. Here's what, now deceased, science fiction writer Michael Crichton said about consensus science in a 2003 speech delivered at the California Institute of Technology(4).

“I regard consensus science as an extremely pernicious development that ought to be stopped cold in its tracks. Historically, the claim of consensus has been the first refuge of scoundrels; it is a way to avoid debate by claiming that the matter is already settled. Whenever you hear the consensus of scientists agrees on something or other, reach for your wallet, because you're being had.

Let's be clear: the work of science has nothing whatever to do with consensus. Consensus is the business of politics. Science, on the contrary, requires only one investigator who happens to be right, which means that he or she has results that are verifiable by reference to the real world. In science consensus is irrelevant. What is relevant is reproducible results. The greatest scientists in history are great precisely because they broke with the consensus."

Corporations are skilled at promoting consensus of scientific opinion. As far as I can tell, countering such tactics is not yet in the skill set of politicians.

References

1. http://freepressonline.net/content/what-has-government-done-our-health

2. http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/fats-full-story/

3. http://www.youtube.com/watch?v=dgU3cNppzO0

4. http://s8int.com/crichton.html

In light of this, perhaps I can contribute, too. Here is an article -- sorry, not primary -- suggesting that poor insulin function within the brain, whether it is caused by insulin resistance or poor insulin receptor function in the neuron. This might eventually lead to the buildup up beta-amyloid plaques, which is the hypothesized (though, not proven) cause of Alzheimer's Disease.

http://nutritionwonderland.com/2010/01/glucose-brain-alzheimers-diabetes/

Neuron no need insulin to capture glucose.

About fructose, I think we are prepared to metabolize slowly. On fruits it is combinated with fiber, and its digestive entrance is slow.

Fructosa from the sucrose disaccharide (normaly sugar), in this form, have a quickly entrance (more than alone, glucose too), and the bad effects of their slowly metabolism are worse.

David Brown, we only can educate the people...

Ana, the article suggests that neurons need insulin in order to survive, although this was not thought to be the case for a long a time. Here's a more recent press covering this research:

http://www.sciencedaily.com/releases/2012/03/120323134908.htm

What should I make of this?

Neuron no need insulin to capture glucose, but the insulin or IGFs have many effects on cell. Signaling cascade of insulin (PI3K, MAPK, AKT, FOXO, mTOR, BDNF, etc.) make very different actions on cell, neuron too. For that if exist resistance of insulin in all cell, they have problems in many regulations of the cell function. Entrance of insulin in brain (blood-brain barrier) is regulated for IR, active transporter. It's possible to make inside too (exist RNA). This is very studied now.

Yes, sugar over consumption, from the material point of view, is one of the most responsible for obesity. I call it "calories bomb" while it has no nutritional value, just energy. The energy needs to be spent. But, nobody should give up sweets and the pleasures of Life.

Keeping it all in balance is the secret.

So, we coming back to the human mind and education, behavior. We, as humans want too much and all at once like there is no tomorrow, so here is the biggest problem at all as far as obesity is concerned.

Sugar? Yes, like I said, it is a "calories bomb" :-)

Keep your "Life sweet" but with no sugar. How? Love each other every moment and that will drop your weight as well. You may then have some deserts, not too much and not too sweet, but don't forget to love yourself and the dear ones.

Keeping your weight off and staying healthy will keep you family, friends and lovers very happy as well by having you around them for long time and in a pleasant fashion, full of vitality. Sugar? Just a bit. Love, as much as your heart can handle. Infinite, that will not get you fat !

Din I answer the question? Thank you for your patience!

With my regards and respect to all RG participant members,

Adrian TW

Bert Hubert is correct. Fructose is a precursor to TG synthesis via de novo lipogenesis. The TG made in the liver is exported as VLDL particles which contain cholesterol and apolipoprotein-B (see refs).

http://www.ncbi.nlm.nih.gov/pubmed/15971409

I agree with Dr Mathias. The increase in obesity can be traced back 30+ years to the increased intake in sugar. As I have stated before the bad guy seems to be fructose which goes primarily to the liver and is metabolized there using up ATP and producing uric acid which is toxic to the kidney and increases inflammatory factors throughout the body. Google Robert Lustig-fructose or read Richard Johnson's book The Sugar Fix for detailed information,.

It sounds like most of us agree that excess sugar intake is the #1 problem. A note of caution, however, Even if sugar consumption is the primary cause of increased obesity, it does not necessarily follow that reducing sugar intake will eliminate obesity. Once a fat cell is created, it seldom dies away. The effects of sugar over-consumption may in part be irreversible. This fits with studies of "post-obese" rodents and humans.

Paul--

Can you elaborate? Seems to me if sugar causes obesity through insulin-dependent storage of fat in the form of triglycerides in adipose tissue, and a decrease in fat storage occurs when triglycerides leave the adipose tissue in the form free fatty acids, then the amount of free fatty acids that leave the cell relates to the size of the fat cell. Is this not the case?

Is your explanation the reason why formerly obese people have 'extra skin'?

Thanks,

Caleb

John Mcneill, your explaination is pointing more or less in the right direction - is the fat around the waist not loaded with toxins.... why are they there ... why are they not neutralized or evacuated ????? Our body is supposed to be self regulating ... what is missing to acheive this ???? Isn't water the only substance our body uses to dissolve waste and toxins ???? Read the book from dr, F Batmanghelidj and you will find the real cause of overweight ......see link attached

http://www.amazon.com/Obesity-Cancer-Depression-Common-Natural/dp/0970245823/ref=sr_1_8?ie=UTF8&qid=1353341312&sr=8-8&keywords=your+body+many+cries+for+water

In my opinion, one cannot hydrate or supplement oneself out of a problem one ate oneself into. Obesity and noncommunicable disease are on the rise throughout the world. To be sure, this is partly due to the fact that more people are hydrating themselves with sweetened beverages. In that case, switching back to water and consuming sea salt might furnish substantial benefit. However, I doubt improper hydration accounts for any substantial portion of new cases of obesity.

As for endurance athletes requiring extreme hydration, South African fitness researcher Timothy Noakes investigated this issue. http://www.humankinetics.com/products/all-products/waterlogged

Dr. Noakes also furnishes an excellent summary of the causes of the obesity epidemic in a recent "South African Medical Journal" article. Quote:

"We have now reached the paradoxical situation: global medical research has grown exponentially, yet it is probable that much public health information propounded as undeniably ‘true" is manufactured to serve the commercial interests of several global industries...I concluded that the cause of the global epidemic of obesity and diabetes is simple; both conditions occur in those who are genetically carbohydrate-resistant but who persist in eating the high-carbohydrate diet according to the US Dietary Guidelines. This interpretation is not novel – it was the standard teaching in most medical schools in Europe and North America, but disappeared when the fallacious diet/heart hypothesis took hold in the 1970s.

But if obesity and diabetes are due to the overconsumption specifically of carbohydrates in those who are carbohydrate-resistant, then their prevention and cure require only that those who are the most severely affected eat a high-fat and -protein diet to which carbohydrates contribute less than 60 g per day. Yet as long as these conditions present massive commercial opportunities to the pharmaceutical and food industries, there will be no appetite for such a simple solution. Our sole recourse is to change the behaviours of those at risk, one meal at a time.

The evidence is tenuous for the related diet/heart hypothesis, which holds that a diet full of ‘artery-clogging saturated fat; causes an elevation of blood lipid concentrations, thus promoting coronary atherosclerosis and ultimately heart attack. I argue that the evidence is essentially non-existent. Opposing this is that coronary heart disease (CHD) is, like obesity and diabetes, an inflammatory disorder caused by abnormal carbohydrate metabolism in those eating a diet low in omega-3 polyunsaturated fats and high in trans fatty acids and omega-6 polyunsaturated fats." http://www.samj.org.za/index.php/samj/article/view/5627/4216

David Brown ...Then maybe you can explain my exel file with results from more then 1500 people .... NOBODY with 66% hydration level has more then 9.8% body fatt mass.. athletic or sedentary .... on the other hand ALL of them with hydration level of 46% has at least 37% fatt mass and ALL of them with hydration level of 34% or less have at least 57% body fat mass ....

My tabel goes from 67% being the highest equals 8.5% body fat mass and 27% hydration level being the lowest and that equals 63.5% body fat mass ...

Female 58 years old and 172 cm tall with 139 kg !!!!!

Why do you find top professional rugby player with 10% BFM and another from same team with 28% BFM , they get the same food, do the same training ( min 5h daily)

If eating had anything to do with it, why are overweight people not healed after strong diet where they lost all the extra weight .???????

Why are all the overweight people back to perfect weight and stay there without one day of diet , just proper hydration until their level was back at 64% or higher ...

And yes we start proper scientific medical research program with our protocol... I read the books and applied the concept and as explained in his books we had the results he claimed ( Dr. F. Batmanghelidj)

All this is from 5 years of coaching people into health... no pills... no diet ... no excercise untill they reach a proper hydration level....

by the way I don't trust scientific research because each researcher will find what the sponsor of the project wants him to find ... or it doesn't get published when inconvenient to sponsor's program. ( business)

John , " The increase in obesity can be traced back 30+ years to the increased intake in sugar." Regarding this statement ....:

I had my first coke at the age of 18 ..... now you see toddlers 3 - 4 years drinking cans of Coke and more then one a day ...

Any idea what a 2.4 pH drink 33 cl carbonated drink full of different acids.. do to a 5 to 8 kg kid ...???? they only have 3 to max 4L of water .... they go into metabolic acidosis right away .... their small body can not handle the toxic load of such a drink ... (sugar loaded to cover up the acids )

Are these data relating hydration status with fat mass obtained from using impedanciometry? Because the machine measures water in the body it is not surprising that the more water one has in the body, the higher the lean body mass (muscle mass) and the lower the fat mass; the other way around also holds true.

Has nothing to do with HOW it is measured ....

57 year old male 180cm tall ... 57kg .. 67% water .. 8.5% fat = 4kg fat

64 year old male 187 cm tall ... 138 kg .. 43,5% water and 40,5% fat 52kg fat

Is only a matter that hydrated person has minimal fat .... even slightly underweight

Dehydrated people are overweight or obese ....

High glycaemic index food is rapidly absorbed in the upper gut, leaving the distal gut with less absorptive work. This is the opposite of what is provoked by fibre.

Looking to the hormonal activity of the bowel, both obesity and type 2 diabetes imply high hormonal activity of the upper gut (high GIP, which generate neither satiety nor the blockage of glucagon secretion), and simultaneously low activity in the distal gut (Low and retarded secretion of GLP-1, PYY, Oxyntomodulin, which are indeed responsible for satiety, insulin secretion and blocking glucagon)

In conclusion, we have a digestive tract not adapted to high glycaemic index food.

We do not need treatment, because the disease is an environmental change.

We need adaptation.

It is interesting to observe how different animals adapt to higher and poorer glycaemic diets.

I attach a short paper about it.

Sérgio Santoro

Sao Paulo, Brazil

The glycemic index (GI) of foods itself is not responsible for the phenomena that Sergio discussed in his reply. Meal-associated circulating glucose and insulin excursions do not appear to have a causative role in the adverse metabolic effects of GI such as increased visceral fat accumulation, lipids and reduced insulin sensitivity (see reference- http://www.ncbi.nlm.nih.gov/pubmed/21613559 ). Rather, it appears likely that it is the low fiber content of high GI diets that is involved in any adverse effects of high GI diets and higher fiber content of low GI diets that is protective against the development of metabolic disease.

Our daily choices represent a VOTE beyond the election day. I invite you to take a stand and express your point of view, more as to address youngsters ( Facebook users ) as well as general people, the consumers.

Please see For the Facebook user, I invite you to participate, LIKE and sign-up: https://www.facebook.com/VoteForLifeOnTerra?ref=hl

Like, subscribe, contribute, comment.

Thanks,

Adrian TW

ok, Adrian

yet

Kamimura et al. Molecular hydrogen improves obesity and diabetes by inducing

hepatic FGF21 and stimulating energy metabolism in db/db mice. Obesity 19(7):13961403

(2011).

Epidemiology is never good at finding out causes, so cannot quite help answering whether sugar consumption is the culprit. But there is a strong correlation, no doubt. And that (together with the more pathophysiological answers given here) should suffice considering testing interventions, and here sugar sweetened drinks are a good target. True the causes of the obesity problem are more complex, but if one component plays a dominant role and can be reduced without too great difficulty, then I think we should all support initiatives to take the sugary drink out of schools etc. Not only in Berlin ;-) Great petition Stefanie I like to support !

I agree with Maximilian de Courten. While epidemiology gives no causal evidence, it gives indications which should be supported by in vitro/in vivo tests. Epidemiologically, gestational diabetes, excessive maternal weight gain (more than 20 kg), maternal BMI, and maternal smoking during pregnancy are all linked to increased risk of overweight/obesity in children. In vivo, pre- and perinatal overfeeding resulted in increased risk for metabolic syndrome, and increased levels of glucose have been linked to altered methylation patterns of the insulin receptor promoter, as well as of the promoter of POMC. This led to insulin and leptin resistance, which was reversible when postnatal feeding was normalized. All in all, the increased availability of macronutrients is at fault for the obesity epidemic, which includes a shift in metabolic disposition towards obesogenic. While all factors cannot be removed from the equation (!), great efforts need to be made to control the largest factors, such as fast food, sweetened beverages, alcohol and smoking. Measures should include education and increased awareness both at the medical levels (doctors, hospitals, health insurance initiatives) and schools.

Sources:

Andreas Plagemann, 2012. Perinatal Programming: The State of the Art. pp. 243-275. Walter de Gruyter & Co. KG, Berlin/Boston.

Guyenet SJ, Schwartz MW. 2012. Clinical review: Regulation of food intake, energy balance, and body fat mass: implications for the pathogenesis and treatment of obesity. J Clin Endocrinol Metab 97: 745-755.

Oken E, Rifas-Shiman SL, Field AE, Frazier AL, Gillman MW. 2008. Maternal gestational weight gain and offspring weight in adolescence. Obstetrics and gynecology 112: 999-1006.

Oken E, Levitan EB, Gillman MW. 2008. Maternal smoking during pregnancy and child overweight: systematic review and meta-analysis. Int J Obes (Lond) 32: 201-210.

Schneider S, Gruber J. 2012. Neighborhood deprivation and outlet density for tobacco, alcohol and fast food: first hints of obesogenic and addictive environments in Germany. Public health nutrition Available on CJO 2012.

We in this discussion know what is to be done, true, but not everyone knows or agrees. I know of numerous cases of obese individuals who have not once been told by their doctors that they should do anything about their weight. Then their joints get surgically replaced, one by one. So the answer is, as you say, education. If the health care providers don´t know, then they must be sensitized and further educated as to the how.

A combined effort between doctors, health insurances, schools, communities and government funding will be necessary to educate people at all socioeconomic levels, but this costs money and energy, since it is necessary for it to occur at all levels.

In this way, I think all answers are correct. However, obesity is a complicated phenomenon. I would like to add somthing to the answers:

1. Now, glycemic load (GL) is more important than glycemic index (GI). GL reffers to increase blood glucose by the whole food items eaten in a meals. Because usually we eat some food items in a meal not only one item like sugar. You may eat a high GI food (i. e. white rice) with vegetables. indeed, you can decrease GI by adding vegetables to foods.

2. You also should consider the role of fats in the diet. When scientists explored the role of fat in obesity, industries tried to produce less fatty foods but more sweetened. Whilst fatty foods helps more satiety. sweetened foods can led to more hungry and eating,

2. Do not forget differences between developing and developed countries. Whilst in developed countries low SES people are at higher risk of obesity (because the buy cheaper foods whit less quality), in developing countries high SES peoples are also at risk because they a lack of knowledge.

As Sheila said, prevention programs cost money . I think the most powerful tool against obesity is knowledge at all levels.

Monireh is right. Knowledge is an powerful problem-solving tool. However, the quality of the knowledge is crucial to the success of the effort. At present, the world is plagued with dietary dogmas that mislead both experts and consumers alike. The problem has to do with corporate relationships with academia and politics. For example: http://www.weightymatters.ca/2012/12/how-food-industry-influences-food-policy.html

I'm not saying corporations are inherently evil. To the contrary, they furnish enormous benefits to society. It's just that they need to be watched carefully. Like all the rest of us, they need to be made aware of their mistakes so they can correct them. http://www.prweb.com/releases/david_brown/omega-6/prweb8933501.htm

When talking epidemiologically it is important to take into account synergism between many risk factors, one among which is high sugar intake. At this moment a lot is known about how fructose could lead to metabolic syndrome. We cannot overlook contribution of high fat and sedentary life style. Also important is the contribution of environmental contaminants, particularly insecticides.

Recent evidence clearly shows a positive link between blood residue levels of insecticides and traits of insulin resistance. Pls refer the article-

http://www.ncbi.nlm.nih.gov/pubmed/22885474

We all know synergism between many risk factors could result in serious problems. Take into perspective what could happen when many risk factors work together. This could explain why incidence of metabolic syndrome is steadily increasing world over.

After I saw the video that David Brown posted... I'd like to share a related video ( http://www.youtube.com/watch?feature=player_embedded&v=ovO18E-hgew ) that show us an alternative way. It's not necessary a gourmet chef working in the school (secondary focus of the news), but a nutricionist, like in Brazil's public school to give a balanced feed.

To avoid obesity, nutricional (re-)education it's essential, besides exercise. To whom is young, it's easier, and would be great if it's habit don't be corrupted at the school (considering a family that feed properly) like's happening in US public school (according to the video).

Nutricional education needs to get into people mind, the school could facilitate giving a menu to suggest what they could give to their kids. This way make possible to the parents learn how they can continue at their own homes. The sooner it starts, the less will be the damage and difficulty to get success.

So, I think that whether we feel that sugar is the single most important contributor to childhood obesity or not, it contributes nothing but increased palatability to our diet and thus is an easy target for reduction. The ready availability of it in our food supply (added even to bread here in the US), means that we can target it for reduction (as we did with salt in an effort to reduce hypertension). Here in NY we have a ban on sweetened beverages being sold in larger than 16 oz servings and a funded study to see its effects. Obesity rates in children were already starting to decrease when the ban was put into effect so measuring its impact will be tricky!

Stephanie and Jo make very good points. I see this problem in my clients everyday. What I did not see mentioned was the rise of diabetes with the introduction of high fructose corn syrup into the food supply. There are many studies which address the effects that HFCS has on the body including liver scarring. Couple HFCS with the high saturated fat, high sodium fast foods it is not hard to understand where the obesity and diabetes epidemic is coming form.

This speaks to Jo's point of what counts as sugar. I think HFCS absolutely does. Refined grains (almost any flour) probably should also count as would fruit juices, honey, agave nectar, etc.

Actually, saturated fat is not the problem(1). More likely, it is the omega-6 industrial seed oils that are raising so much havoc(2). Sadly, the omega-6 debate is still just so much background noise as far as the public is concerned(3). And the vast majority of nutrition researchers and health experts have little to no knowledge of omega-6 research(4). Nor are they aware of the historical roots of the low-fat movement(5). An exception is Dr. Timothy Noakes of South Africa. Here's comment(6) about saturated fats and omega-6 published in Vol 102, No 6 (2012) of the South African Medical Journal:

"We have now reached the paradoxical situation: global medical research has grown exponentially, yet it is probable that much public health information, propounded as undeniably ‘true,' is manufactured to serve the commercial interests of several global industries...Too many medical ‘truths are decided by industries that generate products, especially pharmaceutical agents, on which our profession has become too dependent. This relationship has promoted falsehoods with devastating consequences.
..One instance relates to the causes of obesity and adult-onset (type II) diabetes. In 1963 Campbell showed that the appearance of diabetes in Zulu-speaking urban-dwellers and Indian immigrants to Durban was associated with adopting a diet with an increased sugar intake, also confirmed in other populations. The rising incidence of diabetes occurred within about 20 years of first adopting the ‘white man's diet, in keeping with the classic observations by Price that population health falls immediately as it adopts a diet including refined carbohydrates in the form of sugar and white flour...

The logical conclusion is that the global epidemic of obesity and diabetes over the past 30 years is related to diets containing too much carbohydrate and too little fat and protein. But this possibility is of insufficient interest to be taught in medical schools. Instead the US Dietary Guidelines stress the need to increase the intake of ‘healthy carbohydrate and avoid artery-clogging saturated fats.

I concluded that the cause of the global epidemic of obesity and diabetes is simple; both conditions occur in those who are genetically carbohydrate-resistant but who persist in eating the high-carbohydrate diet according to the US Dietary Guidelines. This interpretation is not novel – it was the standard teaching in most medical schools in Europe and North America, but disappeared when the fallacious diet/heart hypothesis took hold in the 1970s.

But if obesity and diabetes are due to the overconsumption specifically of carbohydrates in those who are carbohydrate-resistant, then their prevention and cure require only that those who are the most severely affected eat a high-fat and -protein diet to which carbohydrates contribute less than 60 g per day. Yet as long as these conditions present massive commercial opportunities to the pharmaceutical and food industries, there will be no appetite for such a simple solution. Our sole recourse is to change the behaviours of those at risk, one meal at a time.

The evidence is tenuous for the related diet/heart hypothesis, which holds that a diet full of ‘artery-clogging saturated fat causes an elevation of blood lipid concentrations, thus promoting coronary atherosclerosis and ultimately heart attack. I argue that the evidence is essentially non-existent.

Opposing this is that coronary heart disease (CHD) is, like obesity and diabetes, an inflammatory disorder caused by abnormal carbohydrate metabolism in those eating a diet low in omega-3 polyunsaturated fats and high in trans fatty acids and omega-6 polyunsaturated fats. This seems logical since diabetes is, next to cigarette consumption, the strongest predictor of CHD risk. A single measure of carbohydrate resistance, blood HbA1c concentration, is also a better predictor of CHD risk than conventional blood lipid measurements."

In general, nutrition science has become corrupted by the agribusiness sector and the notion that scientific consensus is more important than data. Here's the late Michael Crichton's view(7) on the matter:

“I regard consensus science as an extremely pernicious development that ought to be stopped cold in its tracks. Historically, the claim of consensus has been the first refuge of scoundrels; it is a way to avoid debate by claiming that the matter is already settled. Whenever you hear the consensus of scientists agrees on something or other, reach for your wallet, because you're being had. Let's be clear: the work of science has nothing whatever to do with consensus. Consensus is the business of politics. Science, on the contrary, requires only one investigator who happens to be right, which means that he or she has results that are verifiable by reference to the real world(2). In science consensus is irrelevant. What is relevant is reproducible results. The greatest scientists in history are great precisely because they broke with the consensus. There is no such thing as consensus science. If it's consensus, it isn't science. If it's science, it isn't consensus. Period.”

References

1. http://www.docsopinion.com/2012/06/04/the-case-against-saturated-fat/

2. http://evilcyber.com/nutrition/disrobing-dogma-polyunsaturated-fat-and-health/

3. http://www.asbmb.org/asbmbtoday/asbmbtoday_article.aspx?id=18365

4. http://sciencenordic.com/vegetable-oils-promote-obesity

5. http://jhmas.oxfordjournals.org/content/63/2/139.full

6. http://www.samj.org.za/index.php/samj/article/view/5627/4216

7. http://www.s8int.com/crichton.html

I am now convinced that carbohydrate is not the problem, fructose consumption is the problem. Studies have shown that intake of complex carbohydrates is healthy. Intake of high glucose in some studies has been shown to not be deleterius. Intake of fructose of more than 50 g per day results in the effects described above.

John Mcneill is quite correct. Dietary carbohydrate composed of glucose by itself (whether as the free sugar or as part of starches) has little to no adverse metabolic effects compared with fructose which has been demonstrated to have a number of negative metabolic consequences, particularly increases circulating lipids and reductions of insulin sensitivity. Postprandial insulin and glucose excursions resulting from the consumption of dietary carbohydrate composed of glucose do not appear to be linked to adverse metabolic effects on lipids or insulin sensitivity (see article links below):

http://www.ncbi.nlm.nih.gov/pubmed/20388133

http://www.ncbi.nlm.nih.gov/pubmed/19381015

http://www.ncbi.nlm.nih.gov/pubmed/21613559

While I agree that fructose is responsible for several of the adverse outcomes in sugars intake as noted by Peter Have and John Mcneil, individuals with type 1 diabetes have several complications associated with elevated glucose levels that are reduced when glucose levels are well controlled. To me that indicates that glucose has adverse effects independently of fructose. I do not think we understand the additive or multiplicative effects of these sugars but that each have adverse effects, perhaps through independent mechanisms. From a practical perspective, reducing the intake of sucrose with consequent reduction in both glucose and fructose makes sensible advice to prevent or treat metabolic syndrome.

Dr. McNeill, you have put it across in a perfect way.

Obesity is an indirect result of mental attitude as response to external factors. Also, financial interests are pushing products creating demand for calories over-consumption. We need to observe the bioeconomic principles in out human endeavors for a healthy future. Search Google on " Triangular EcoKinematics Theory " describing an equilibrium principle for Life, known to be in disequilibrium. How one influences the other and why. Videos and PDF are available at different links.

Oh, on bioeconomics, here is the PhD full public presentation video with comments, etc. Enjoy. Comments are welcomed on the link. Please propose eventual collaboration by sending private messages.

http://youtu.be/FBo5dz-rGyU

Regards,

Adrian Toader-Williams, PhD.

USA - Romania

Full active member of the International

Academy of Science, Russian Section

Moscow, Russian Federation

So, what if we were to regard glucose/fructose/sucrose in the same way as we do essential vitamins, since they, too, have a U-shaped curve in that the brain is dependent on glucose, but too much has negative health effects. Essential vitamins have an RDI but also a ceiling intake level. In addition, food additives and pesticides have ADIs (Accepted Daily Intake values) which are calculated based on long-term exposure and for specific endpoints, such as neurotoxicity. The industry is bound by law to keep substance amounts in food lower than what would cause human exposure to exceed the ADI.

An ADI or ceiling intake could be calculated for glucose and/or sucrose/fructose with the endpoint of insulin resistance, let´s say, with HOMA as the indicator and a benchmark dose level 10 (BMDL10) as the reference point. Then the industry could be bound by law to keep levels below the levels that would cause exposure to exceed this level.

I realize it wouldn´t be as simple as I´m making it sound, especially the binding by law of the industry, but also the necessity for animal experiments with fairly large study groups to account for highly variable metabolism. However, more control of the adding of any or all of these sugars at the level of industry is going to be necessary if the obesity epidemic is going to be solved. This way, the solving of the problem wouldn´t be as dependent on doctors´ telling their patients to eat less and move more and the patients sticking to it.

My opinion on this is very simplistic; If calories out are the same as calories in then you won't gain weight. Sure surgar consumption has increased a lot of the past few decades, especially with the introdution of high fructose corn syrup etc but at the end of the day diet composition is irrelevant as the laws of thermodynamics cannot be broken. I understand the idea that over consumption of sugar leads to increased adipogenesis and fructose drives lipid accumulation in the liver, and insulin/leptin resistance in the brain causes further over eating - but so long as an individual is in caloric balance none of that matters. Its all well and good making broad statments about what has caused obesity at the population level but to cure the epidemic we need individualised approaches in combination with what Shela Elz suggests like legislative regulation on the amount of sugar - especially in soft drinks.

Richard Mathias is correct in that in Type 1 diabetes control of glucose intake is important. My remarks were directed at obesity and Type 2 diabetes. David Hamilton does not take into account the toxice effects of fructose ingestion as outline by Lustig. Fructose is now held responsible for the increase in non-alcohol induced liver disease and kidney disease. The metabolism of fructose by the liver uses up tremendous amounts of ATP and the resulting increase in adenosine leads to an increase in uric acid. Whether calories are the same is the subject of some debate. But a calorie producer that is also toxic creates additional problems.

Thanks for a great peice of input John Mcneill. I agree that when fructose is in excess in combinatin with excees calories it can by toxic - also via the induction of lipogenic programs. However, I very much doubt that fructose in high levels on a calorically balanced diet would cause any harm but perhaps a trial needs to be carried out to test this. In fact I would argue that a calorically balanced diet high in fructose would be benefical for glucose homeostasis and insulin sensitivity as it has a very low glyceamic index - the majority of it is taken up by the liver from the gut and doesn't make it into the circulation and therefore does not cause anywhere near the same induction in insulin secretion that the equivalent dose of glucose would. But again - perhaps this should be the subject of a trial instead of my speculation.

It may not be so much the fructose as the individualized response to large amounts of it. In other words, vulnerability is a major issue(1). In addition high fructose intake is especially risky when intake of omega-6 lenoleic acid is also high(2). It's important to recognize that many noncommunicable disease conditions characterized as epidemic have increased in lock step with the proliferation of industrial seed oils(3). Yet the omega-6 debate centers around the effects of polyunsaturated fatty acids on cholesterol levels(4,5). Meanwhile, the toxic effects of excessive omega-6 intake are ignored(6).

Notes and references

1. "It was necessary to raise the daily carbohydrate intake to 85-90% of the total daily caloric intake in order to induce hyperglyceridemia in normolipemic subjects."

http://ajcn.nutrition.org/content/20/2/116.abstract

2. "Liver damage with fat accumulation is very common in the United States. According to the NHANES health and nutrition surveys, in the time period 1999-2002, 8.9% of Americans had elevated ALT. Just 10 years earlier (1988-1994), the number was 4.0%. Fatty liver is a growing epidemic that currently affects roughly a quarter of Americans."

http://wholehealthsource.blogspot.com/2009/06/fatty-liver-reversal.html

3. "A revolution has occurred. For instance, in the early 1980s, no adults in China consumed what we call a high-fat diet with more than 30 percent of their calories from fat. Today, over half of Chinese adults consume such a diet. In China, dietary shifts are very quickly occurring. Rice and flour intake is down, and animal-source foods such as pork and poultry and fish are way up, and the steepest increase is in the use of edible vegetable oils for cooking.

People are eating more diverse and tasty meals; in fact, edible oil is a most-important ingredient in enhancing the texture and taste of dishes. The same is true for added sugar. The question is how much."

4. "In 1965, Keys and his colleagues at the University of Minnesota published an equation that quantified the relationship between saturated fats, polyunsaturated fats and serum cholesterol levels (2). The equation helped to sway public health dietary emphasis toward the polyunsaturated fats, which include EFAs, to lower blood cholesterol levels. But the Keys equation treated all unsaturated fats the same. It didn’t distinguish between omega-3s and omega-6s."

http://www.asbmb.org/asbmbtoday/asbmbtoday_article.aspx?id=18365

5. http://www.hsph.harvard.edu/nutritionsource/fats-full-story/

6. http://evilcyber.com/nutrition/disrobing-dogma-polyunsaturated-fat-and-health/

YOu are correct in much of what you have said and at one time some people recommended that diabetics use fructose rather than glucose. The problem as I alluded to in my earlier answer is that glucose goes to every cell in the body. Fructose goes primarily to the liver. Glucose uptake and metabolism is regulated by transporters and by feedback mechanisms while fructose metabolism is not. As stated it is estimated by Richard Johnson that more than 50 g of fructose/day is toxic because the first step in metabolism is phosphorylation from ATP in the liver. When ATP is depleted this is toxic to the liver cell. In addition uric acid is produced which has addtional toxic effects. I again recommend that everyone go on U Tube and listen to the lecture by Robert Lustig on fructose intake, I am sure you will be convinced.

Sadly, Robert Lustig has yet to pay attention to the omega-6/fatty liver disease issue. Scientific evidence suggests that saturated fats protect the liver from the toxic effects of high fructose intake while omega-6s exacerbate the condition(1, 2).

1. http://wholehealthsource.blogspot.com/2009/04/excess-omega-6-fat-damages-infants.html

2. "In 1985, a multi-national study showed that increased SAFA consumption was inversely correlated with the development of liver cirrhosis, while PUFA consumption was positively correlated with cirrhosis."

http://principleintopractice.com/2012/08/02/liver-saving-saturated-fats/

Here is the latest study that I came across regarding glucose/fructose in the diet.

University of Oxford

Study finds that countries that use HFCS in their food supply have a 20 percent higher prevalence of diabetes than countries that don't use HFCS.

A new study indicates that large amounts of high fructose corn syrup (HFCS), a sweetener found in national food supplies across the world, may be a contributory factor to the rising global epidemic of type 2 diabetes.

The study by researchers from the University of Oxford and the University of Southern California reports that countries that use HFCS in their food supply had a 20 percent higher prevalence of diabetes than countries that did not use HFCS. The analysis also revealed that HFCS's association with the “significantly increased prevalence of diabetes” occurred independently of total sugar availability and obesity levels.

The paper reports that out of 42 countries studied, the United States has the highest consumption of HFCS per head of population at a rate of 25 kilograms or 55 pounds per year. The second highest is Hungary, with an annual rate of 16 kilograms or 46 pounds per head of population. Canada, Slovakia, Bulgaria, Belgium, Argentina, Korea, Japan and Mexico are also relatively high HFCS consumers. The United Kingdom was among the countries with much lower levels of consumption—at less than 0.5 kilogram per head of population.

Countries with a higher use of HFCS had an average prevalence of type 2 diabetes of 8 percent compared to 6.7 percent in countries not using HFCS, says the study.

“This research suggests that high fructose corn syrup can increase the risk of type 2 diabetes, which is one of the most common causes of death in the world today,” said Professor Stanley Ulijaszek, director of the Institute of Social and Cultural Anthropology at the University of Oxford, who coauthored the study.

The article published in the journal Global Public Health proposes that the link is probably driven by higher amounts of fructose in foods and drinks containing HFCS. Fructose and glucose are both found in ordinary sugar (sucrose) in equal amounts, but HFCS has a greater proportion of fructose. The higher fructose content makes HFCS sweeter and provides processed foods with greater stability and a better appearance because it produces a more consistent browning when foods made with higher fructose are baked.

Professor Ulijaszek said: “Many people regard fructose as a healthy natural sugar from fruit, and that's true. Natural fructose found in fruit for example, is fine: The 10 grams or so of fructose in an apple is probably released slowly because of the fibre within the apple and because the fructose is inside the cells of the apple. But a number of studies have shown that high intakes of non-fruit based fructose is especially difficult for the body to metabolise, and is a risk for type 2 diabetes because fructose and sucrose are not metabolically equivalent. Our study shows an ecological relationship that suggests there are potential risks in consuming high levels of high fructose corn syrup.”

Principal study author Michael I Goran, professor of preventive medicine at the Keck School of Medicine at USC, said: “The study adds to a growing body of scientific literature that indicates HFCS consumption may result in negative health consequences distinct from and more deleterious than natural sugar.”

I am not a fat expert but I did not see any specific evidence in the references you cited as showing that saturated fats protect the liver from the toxic effects of fructose. I certainly agree that almost everything we beleive about fats,cholesterol and health is wrong as Gary Taube's has outlined in his articles. He also showed that Keys and his colleagues were dead wrong in their assessments of what fats do and this is what lead to low fat diets with the fat replaced by sucrose/fructose (low fat foods) which in turn correlates with the epidemic of obesity, metabolic syndrome, liver disease, hypertension etc. The effects that you suggest for saturated fats may be true but I need to see the data. Some other thoughts on some of the information that you cited. The Pima indians did not have fructose in their diets before contact with the outside wordl. Neither did the Japanese. I am not sure if fructose intake has increaed in China along with meat intake but I suspect it has. Some argue that animal data with fructose does not relate to the human condition because you have to give rats a 60% fructose diet to produce adverse effects. However rats and most animals have the enzyme uricase which breaks down the uric acid formed from fructose metabolism. Humans are one of a very few species that do not have uricase and must get rid of uric acid by excretion. If you inhibit uricase in rats you can produce the effects of fructose toxicity with very low doses of fructose. In any case I look forward to seeing more data on fructose/fat interaction in the literature.

James, I agree with this study almost completely. However the actual difference between HFCS and sucrose is very small. Sucrrose is 50:50 fructose/glucose and HFCS is usually 55:45. The big diffence is the price.HFCS is cheap relative to sucrose so we can now have 52 oz soft drinks and HFCS added to practically everything that we eat. The introduction of HFCS has definitely been responsible for the total increase in fructose consumption.

John Mcneill you make some interesting points here. I wonder if you have any papers you could reccomend to show that fructose depletes ATP in liver cells. Phosphorylation is the first and one of the rate limiting steps in glucose oxidation and it does not cause ATP delpletion, also I find it hard to reconcile that a metabolisable substrate like fructose could actually deplete ATP and that this would be negative - after all part of the benefical action of metformin is via ATP depletion due to Complex 1 inhibition. Additionally, have you any evidence that Pima, indians and the Japanese did not have fructose in their diets prior to contact with westerners - didn't they consume fruit of any description?

John, I tell my clients to avoid as much processed food as possible. This eliminates the both fructose and HFCS from their diets. But I think it is not just the addition of Fructose and HFCS to the foods as you correctly noted. I think it is the sum total of fructose that has displaced sucrose in the diet. Small amounts of fructose or HFCS may not cause a great deal of harm to the body. I think it is the constant influx of HFCS into the body is the problem.

For David, please look at several of the recent reviews written by Richard Johnson re: the depletion of ATP by fructose. The phosphorylation of glucose is regulated by feedback mechanism while the the phosphorylation of fructose is not (Johnson also discusses this). Given where the Pima Indians live I do not think that there is much in the way of fruit available. Prior to the incdreased availability of sucrose beginning at he end of the US civil war humans in general had limited exposure to fructose. The small amount of fruit and honey consumed did not cause a problem. The introduction of cheap HFCS in the 1970s increased the consumption of fructose considerably and has been related to the problems that we are discussing. James, this statement is also in agreement with your comment on fructose intake. However a large acute intake of fructose such as the amount found in a 52 ounce bottle of soda is not good for you!

I was looking through my archive of articles and found this study from 2008.

Fructose Consumption as a Risk Factor for NAFLD

NON-ALCOHOLIC FATTY LIVER DISEASE, NAFLD, HEPATIC STEATOSIS - Fructose, High Fructose Corn Syrup, Soft Drinks, Diet, Insulin Resistance, Diabetes, Obesity

"Fructose consumption as a risk factor for non-alcoholic fatty liver disease," Ouyang X, Cirillo P, et al, Journal of Hepatology, 2008; 48(6): 993-999. (Address: Manal F. Abdelmalek, Division Gastroenterology & Hepatology, Section of Hepatobiliary Disease, Duke University Medical Center, Durham, USA. E-mail: [email protected] ).

In a study involving 49 patients with biopsy-proven NAFLD without cirrhosis and 24 healthy controls, consumption of fructose was found to be 2- to 3-fold times higher among patients with NAFLD, as compared to controls. Patients with NAFLD were found to consume 365 kcal of fructose, compared to 170 kcal per day by controls. Increased hepatic mRNA expression of certain enzymes necessary for fructose metabolism (fructokinase) and lipogenesis (fatty acid synthase) were found among patients with NAFLD. The authors point out that the rise in NAFLD coincides with a significant increase in fructose consumption, particularly in the form of high fructose corn syrup, found in soft drinks among other sweetened foods. The authors conclude, "The pathogenic mechanism underlying the development of NAFLD may be associated with excessive dietary fructose consumption."

I agree. I heard a seminar this week at my university by Eric Yoshida, a liver expert, who said the same thing.

Maybe it is time to take HFCS off the market.