Big Fat Myths by Ruben Meerman
Ruben Meerman and Professor Andrew Brown from the School of Biotechnology and Biomolecular Sciences, University of New South Wales published a paper in 2014 When somebody loses weight, where does the fat go? 1 Professor Brown specialises in the study of lipids (fats) including cholesterol. Meerman has a physics degree and is known as the surfing scientist and has appeared in a number of television shows including ABC’s Catalyst program. He is the author of Big Fat Myths, a book that expands on the previous paper. The original paper and later book explains how every molecule of fat escapes the human body during weight loss. 2
According to Meerman,
Excess carbohydrates are NOT converted to fat, except in forced circumstances. Excess sugars and carbohydrates are stored as glycogen in the liver and muscle cells. This is why athletes perform “carbohydrate loading” to build up there store of glycogen before endurance events. “Hitting the wall’ occurs when these stores are depleted.
Professor Stewart Truswell, professor of Human Nutrition at University of Sydney, explains: “In some animal species, carbohydrates in excess of requirements are converted to fat via the pathway of lipogenesis. […]. Other than in the experimental situation of gross carbohydrate overfeeding, conversion of carbohydrate to stored lipids does not occur to any appreciable extent in humans.” 3
Marc Hallerstein, professor of Nutritional Science at Berkeley: “Fat cannot be converted to carbohydrate in animals because animals lack the enzymes of the glyoxylate pathway, and carbohydrate is not converted to fat because of a functional block of uncertain cause.” 4
He also states, “Under most dietary conditions, the two major macronutrient energy sources (CHO and fat) are therefore not interconvertible currencies; CHO and fat have independent, though interacting, economies and independent regulation.” 5
A research team at University of Lausanne: “These findings challenge the common perception that conversion of CHO to fat is an important pathway for the retention of dietary energy and for the accumulation of body fat.” 6
According to Meerman and Brown:
The body has complex feedback mechanisms which allow us to maintain homeostasis – a dynamic static of equilibrium that ensures a multitude of variables remain within a functional and viable range. This includes body temperature, electrolyte balance and body weight. The minerals in our blood need to be maintained within a very narrow range which is normally achieved despite a wide variation in their consumption. The idea that our “weight-loss strategy is easily foiled by relatively small quantities of excess food” just does not apply in the real-world.
One well-known study showed that ADDING 12 slices of white bread (at 70 calories a slice) or high-fiber bread (at 50 calories a slice) to existing diet of overweight participants (a diet that resulted them in being overweight in the first place), resulted in an average weight loss of 9 kg over a period of 8 weeks. There was no change in their physical activity or exercise. 7
Meerman and Brown states that:
The Lifson paper was studying the source of oxygen in respiratory carbon dioxide after oxidation of glucose. Oxidation of fats and proteins were not considered in this study. 8
Meerman and Brown seem to ignore the fact that carbon dioxide that we exhale is also created during oxidisation of glucose – which is why blood sugar and glycogen stores are lowest early morning. They make the fundamental mistake of assuming that the carbon dioxide we exhale is produced only from the metabolism of fats.
The conclusion of the paper states:
This advice simply does not work. Not surprisingly, what you eat has an enormous impact on your health and weight – far behind the simple (simplistic) advice of “eat less, move more.”
For example, “An overwhelming amount of evidence shows that the ratio of fat to carbohydrate in the diet is the primary factor in the macronutrient composition of the diet that easily causes passive over-consumption of energy and thus leads to weight gain. In contrast, high-carbohydrate diets seem relatively benign, regardless of the type of carbohydrate.” 9
Reasons why a complex carbohydrate-based (that is, starch-based) diet leads to greater weight loss are: 10 11
- Fats are more readily absorbed from the intestine than carbohydrates.
- Fats are much more energy dense – the same volume of fats contain 2¼ times more energy than carbohydrates. Also, because they take less volume, they are not as filling so we eat more.
- The energy costs of digesting carbohydrates are much greater than fats – we expend much more energy to digest carbohydrates than we do to digest fats.
- People on a predominately plant-based diet have a higher body temperature than those on a animal-based diet. People on a ketogenic diet, have a lower body temperature. Raising the body temperature expends more energy.
The National Weight Control Registry (NWCR) was established in 1994. It is the largest study into long-term weight loss programs. The principal researchers are Rena Wing (Brown Medical School, Rhode Island) and James Hill (University of Colorado). There are now over 10,000 participants enrolled in the study. 12 13
To be eligible to enroll in the study participants must be at least 18 years old, have lost at least 13.6 kg (30 lbs) of weight and kept it off for at least one year.
According to the researchers “almost nobody is on a low-carbohydrate diet” and they have looked “very hard to locate them.
The suggestions from the NWCR to successfully maintain a healthy weight-control program are:
- engaging in high levels of physical activity
- eating a diet that is low in calories and fat
- eating breakfast
- self-monitoring weight on a regular basis
- maintaining a consistent eating pattern; and
- catching “slips” early
Last updated on Saturday 3 December 2022 at 15:20 by administrators
Footnotes
- Meerman, R. & Brown, A. J. (2014) When somebody loses weight, where does the fat go? BMJ. 349 (dec16 13), g7257–g7257.
- Meerman, R. (n.d.) Ruben Meerman [online]. Available from: https://rubenmeerman.com/ (Accessed 7 September 2018).
- Mann, J. & Truswell, A. S. (eds.) (2017) Essentials of Human Nutrition. Fifth Edition. London: Oxford University Press.
- Hellerstein, M. K. (2001) No common energy currency: de novo lipogenesis as the road less traveled. The American Journal of Clinical Nutrition. 74 (6), 707–708.
- Hellerstein, M. K. (1999) De novo lipogenesis in humans: metabolic and regulatory aspects. European Journal of Clinical Nutrition. 53 (1), s53–s65.
- Acheson, K. et al. (1982) Glycogen synthesis versus lipogenesis after a 500 gram carbohydrate meal in man. Metabolism. 31 (12), 1234–1240.
- Mickelsen, O. et al. (1979) Effects of a high fiber bread diet on weight loss in college-age males. American Journal of Clinical Nutrition. 32 (8), 1703–1709.
- Lifson, N. et al. (1949) The Fate of Utilized Molecular Oxygen and the Source of the Oxygen of Respiratory Carbon Dioxide with the Aid of Heavy Oxygen. Journal of Biological Chemistry. 180 (2)
- Saris, W. H. (2003) Sugars, energy metabolism, and body weight control. American Journal of Clinical Nutrition. 78 (4), 850S-857S.
- Bell, E. A. et al. (1998) Energy density of foods affects energy intake in normal-weight women. The American Journal of Clinical Nutrition. 67 (3), 412–420.
- Astrup, A. (2001) The role of dietary fat in the prevention and treatment of obesity. Efficacy and safety of low-fat diets. International Journal of Obesity. 25 (S1), S46–S50.
- The National Weight Control Registry (n.d.) National Control Registry [online]. Available from: www.nwcr.ws/ (Accessed 26 September 2017).
- Wing, R. R. & Phelan, S. (2005) Long-term weight loss maintenance. The American Journal of Clinical Nutrition. 82 (3), 222–225.
4 Replies to “Big Fat Myths by Ruben Meerman”
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Deception from The BMJ
The original article “Big Fat Myths by Ruben Meerman”, lists four references stating that lipogenesis is not a major metabolic pathway. References [3]-[6]. There are many, many more references in peer-reviewed medical journals stating a similar conclusion.
As Marc Hallerstein, professor of Nutritional Science at Berkeley wrote: “Fat cannot be converted to carbohydrate in animals because animals lack the enzymes of the glyoxylate pathway, and carbohydrate is not converted to fat because of a functional block of uncertain cause.” [4]
“These findings challenge the common perception that conversion of CHO to fat is an important pathway for the retention of dietary energy and for the accumulation of body fat.” [6]
A 17 page booklet is available to download from my web site from a link in the right panel.
The book describes JS Sweeney experiments of 1927 and 1928 that compares four highly improbable diets.
* very high-carbohydrate diet
* very high-fat diet
* very high-protein diet
* a fasting regime
The students were fed their diets for two days and a glucose tolerance test was performed on the morning of the third day. After only two days on their experimental, improbable diets, the only group showing a normal, healthy response to the glucose tolerance test was the high-carbohydrate group. A graph is shown that clearly displays the results.
Sir Harold Himsworth published a number of papers in the 1930s that demonstrated that “a low proportion of carbohydrate and a high proportion of fat were associated with a high incidence [of diabetes].”
It was not until the mid 1990s that the mechanism for insulin resistance was discovered. Type “intramyocellular lipids diabetes” into a Google Scholar search, you will receive hundreds of search results that documents the cause of type 2 diabetes. “Intramyocellular lipids diabetes” refers to fats inside muscle cells. Many of these papers stress that changes in the “intramyocellular lipids” can occur overnight and occurs in lean trial participants. Full details are found within the document along with the references.
Read the “Taiwanese Buddhist Study” web page. It shows how a tiny amount of animal-sourced food can have a big impact on diabetic outcomes. The article shows the data.
View the “Rural Indian Regional Diets” article. Despite India’s reputation for a healthy, vegetarian cuisine, it is not justified. Only 1.6% of Indians are vegan, 24% are lacto-vegetarian. 3% add eggs to their lacto-vegetarian diet which leaves 72% consuming meat. The Indian diet is not a low-fat diet or low-animal based diet. Some regions consume a very high level of dairy products.
There are wide variations of diet in India. This is documented in the article. Rice and wheat consumption varies significantly. There is a wide difference between rural and urban health outcomes and the health between different dietary regions. The diet of the south-west is significantly influenced by the Portuguese. The northern regions and Gujarat have a particularly high level of dairy products. Added oils are a significant contribution to the Indian diet.
There is much more information in the article.
The amount of macro-nutrients (fat, carbohydrate, protein, sugars or saturated fat) is not a measure of how healthy a diet is.
None of this does not suggest that a diet high in sugar is healthy. However, it does not cause diabetes (or heart disease or auto-immune diseases).
A healthy, whole-food, plant-based diet is high in complex carbohydrates, low in fats, saturated fats and sugars as well as being high in fibre, anti-oxidants and a multitude of micro-nutrients that work synergistically.
Further to my comments:
In iINDIA, lots of people are vegetarians, they eat lots of carbohydrates ( rice) ,sweets and hardly any fat, have big abdomens , so lots of abdominal fats which come from conversion of carbohydrates in fats and become diabetics.
Kind regards,
R.Ramtohul,
France
About : “Excess carbohydrates are NOT converted to fat, except in forced circumstances. Excess sugars and carbohydrates are stored as glycogen in the liver and muscle cells.”…..In physiology, i have been led to believe that the body does not have enough space in liver and muscles to store glycogen. The excess carbohydrates are obviously stored as triglycerides.
Also, the glycogen is more readible availableand more quickly to reach and metabolise than tryglycerides for energy. This can explain why athletes resort to carbohydrate loading.
Also about sugars and insulin resistance…In times of famine, the body seemed to have found ways to store energy in this following way, it seems: When food is plentiful, the body would not metabolise all the carbohydrates..It will convert them partly in glycogen to be stored in liver and muscles to be readily available for energy with the help of insulin.;;But as there is not enough space for glycogen, the body would store most of the carbohydrates as tryglycerides which are more compact to store , everywhere as subcutaneous fat, fats around organs such as liver, heart ..etc. But for the body to do that, it has to make insulin less effective and not metabolise the excess carbohydrates. This idea of insulin less effective is..”insulin resistance”. So through evolution , human have developed genes of insulin resistance. These genes remain dormant, but the excess fat , especially, large volume of abdominal fat, will ” wake up” these insulin resistance genes especially around the age of 45 years and dabetes (type 2) will manifest itself. As there are no longer times of famine in the world as in ancient ages, diabetes type 2 is prevalent more in humans who eat more than their bodies require and who have big abdomens;
The advices -get rid of the fat, by eatng less, more excercises and proper breathing- through life are justified and can help to get rid or prevent diabetes
Humans with big abdomen invariably become diabetic type 2.
Kind regards
Your post only just came to my attention and, considering the effort you put into writing it, I thought you might still appreciate a response even it is perhaps two years too late. We are hopefully on the same team, after all, doing our best to improve the health literacy of our fellow citizens, and each other.
My objective is to educate people that the carbon atoms they consume as macronutrients are exhaled as carbon dioxide (apart from the tiny fraction excreted in urea and other dissolved urine solids). I am not trying to educate people which diet is healthiest or best for them because that is not my expertise.
I am very familiar with the McDevitt study referred to in the 2001 Hellerstein editorial you quoted, and I agree that our wording does not reflect all of the intricacies of de novo lipogenesis, such as the increase in carbohydrate oxidation and decrease in fat oxidation during overfeeding on a mixed diet, etc. The BMJ provided us with 850 words, so it was impossible to include all of the nuance.
Your suggestion that there is essentially no de novo lipogenesis in the human body, however, is incorrect and based on outdated references (you cite Hellerstein, 2001; Hellerstein, 1999; Acheson, 1982).
I therefore refer you to the more recent work of Schwarz et al (2003), Strawford et al (2004), the reviews by Ameer et al (2014) and Sanders & Griffin (2016), and other works cited therein (references below).
I also notice that you are quoting the 5th edition of Stewart Trusswell’s textbook, which sounds like it might be in need of some revision.
Regarding our muffin, I am not quite sure what point you are trying make with the high fibre diet study (Mickelsen et al 1979). We are not commenting on the healthfulness (or lack thereof) of different diets, or to the effects on satiety of different kinds of foods
Our point might have been clearer if I had avoided using the word “energy” and stayed focussed on how many grams of digestible carbon atoms there are in e.g. a muffin compared to how many grams of carbon atoms a person exhales per minute during physical activity in excess of how many are exhaled at rest.
Relatively small quantities of excess carbon atoms in the diet do contribute to a person’s mass until they are exhaled as carbon dioxide, because all of our mass comes from atoms. I am not quite sure but it seems that you somehow disagree with this?
Your assertion that Lifson was only studying the oxidation of glucose and ignored the oxidation of fat and protein is incorrect. Lifson et al used glucose as their example to explain that at least some of the oxygen atoms in exhaled CO₂ must come from a source other than the glucose itself, but then add that, “Similar considerations with differences in details would be expected to apply to the complete oxidation of fats and proteins.” (see page 804, last sentence of first para).
I am surprised by your assertion that we, “make the fundamental mistake of assuming that the carbon dioxide we exhale is produced only from the metabolism of fats”, because, in fact, we explicitly stated that we used a respiratory quotient of 0.8 in our calculations. Perhaps you were not seeing the forest for the trees?
Finally, we are not advocating one kind of diet over another. We are simply pointing out where the atoms go during weight loss and that the one thing that all successful weight loss diets have in common (whether they are “healthy” diets or not) is that more atoms come out of the body than went back in. I hope you would agree with that?
I hope this goes some way toward clearing up your concerns but I’d be more than than happy to provide you with further information.
Kind regards,
Ruben
REFERENCES:
Ameer F, Scandiuzzi L, Hasnain S, Kalbacher H, Zaidi N. De novo lipogenesis in health and disease. Metabolism. 2014 Jul 1;63(7):895-902.
Sanders FW, Griffin JL. De novo lipogenesis in the liver in health and disease: more than just a shunting yard for glucose. Biological Reviews. 2016 May;91(2):452-68.
Schwarz, J.M., Linfoot, P., Dare, D. and Aghajanian, K., 2003. Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate isoenergetic diets. The American journal of clinical nutrition, 77(1), pp.43-50.
Strawford A, Antelo F, Christiansen M, Hellerstein MK. Adipose tissue triglyceride turnover, de novo lipogenesis, and cell proliferation in humans measured with 2H2O. American Journal of Physiology-Endocrinology and Metabolism. 2004 Apr;286(4):E577-88.