Archive for the ‘Weight Control’ Category

Obesity can lead to vitamin D deficiency

Wednesday, February 6th, 2013

obesityTUESDAY Feb. 5, 2013 — Obesity can lead to vitamin D deficiency, a new study indicates.

British researchers looked at data from about 165,000 people, and found that a 10 percent rise in body-mass index (BMI) was linked with a 4 percent drop in concentrations of vitamin D in the body. BMI is a measurement of body fat based on height and weight.

The link between BMI and vitamin D levels was found in men and women, as well as in younger and older people, the investigators noted.

The findings suggest that a higher BMI leads to lower levels of vitamin D circulating in the body, while a lack of vitamin D has only a small effect on BMI, according to the authors of the study, published Feb. 5 in the journal PLoS Medicine.

Efforts to tackle obesity may also help reduce levels of vitamin D deficiency, said lead investigator Dr. Elina Hypponen, of University College London’s Institute of Child Health.

Previous studies have linked vitamin D deficiency with obesity, but it wasn’t clear whether a lack of vitamin D triggered weight gain or whether obesity led to vitamin D deficiency, the study authors noted in a university news release.

Vitamin D, which is essential for healthy bones and other functions, is produced by the skin when exposed to sunlight. It can also be obtained through foods and supplements.

“Vitamin D deficiency is an active health concern around the world. While many health messages have focused on a lack of sun exposure or excessive use of suncreams, we should not forget that vitamin D deficiency is also caused by obesity,” Hypponen said.

“Our study highlights the importance of monitoring and treating vitamin D deficiency in people who are overweight or obese, in order to alleviate adverse health effects caused by a lack of vitamin D,” she added.

Although the study reported that higher BMI leads to lower levels of vitamin D circulating in the body, it did not prove a cause-and-effect relationship.

More information

The U.S. National Institutes of Health, Office of Dietary Supplements, has more about vitamin D.


Friday, July 6th, 2012

Conventional wisdom on staying skinny seems to change with every day of the week—but the metabolism-boosting value of healthy snacking throughout the day is a common thread you’ll find running through just about every piece of diet advice out there.

Until now, that is.

That’s right: New research out of the University of California San Diego is shedding a dubious light on the good sense of “grazing”… with results suggesting that it may not be the foolproof weight loss strategy you think it is. {{{0}}}

Fasting Longer Can Keep You Stronger and fitter

The study, published in the journal Cell Metabolism just this past May, analyzed two sets of mice of matching gender, age and genetic makeup. Researchers fed both groups a high-fat diet, allowing one group to eat whenever they wanted—consuming roughly half their food during their waking hours in the evening, and the other half as “snacks” throughout the day—while the other group of mice was restricted to eight-hour eating periods each night, and 16-hour fasting periods through the day. Two control groups ate a typical diet, comprised of only 13 percent calories from fat (as compared to 60 percent in the high-fat experimental groups).

After 100 days, the mice that grazed on high-fat food throughout the day not only put on weight, they also developed high cholesterol, high blood sugar, poor motor control and liver damage. Surprisingly, however, the mice that ate the same amount of high-fat food under time restrictions weighed a substantial 28 percent less—and showed none of the diet-related health declines of their continually snacking counterparts.1

What’s more, the time-restricted mice performed better on exercise tests than both the high-fat grazers and the mice on a normal diet, indicating that extended fasting periods don’t just counteract the devastating effects of gut-busting dietary habits—they might actually play a critical role in keeping you fit, no matter how you eat.2

Scheduled Eating Helps Your Body Heal

This study may not be a golden ticket to a junk food free-for-all. But the results do suggest that the numbers on the scale may have less to do with your nutrition—and more to do with your body’s natural metabolic cycles and circadian rhythms—than once thought.

The researchers found that constant eating leads to constant generation and storage of fat, putting stress on your liver and raising blood sugar. Even a few hours of fasting, on the other hand, is enough to initiate fat-burning and cholesterol breakdown—while putting the brakes on glucose production and giving the body a chance to repair itself and generate new DNA. And this, in turn, alleviates disease-promoting inflammation for a leaner and longer life.

Obviously, this marks a serious departure from your usual diet-focused weight loss discussions. Still, while the findings of this particular study could be game changing, it’s too soon to say if the same results will apply to human subjects. But, in the meantime, simply closing up your kitchen a few hours earlier—and doing away with all impromptu snacking, especially on high-fat, sugary foods—might just prove to be the fat-burning breakthrough you’ve been looking for.




Surgical management of obesity

Saturday, November 20th, 2010

In this article we will discuss the surgical treatment of obesity which is the last resort in resistant weight control. This will conclude our thread on Resistant Weight Control. We will be starting a new thread next month and we hope you have enjoyed our series on this global epidemic that is now getting to be known as “GLOBESITY”.

Surgical treatment of obesity is also known as bariatric surgery or weight loss surgery. Surgery is currently the most effective treatment for morbid obesity resulting in durable and sustainable weight loss and accompanying health improvements.{{{*}}}

Classifications of Surgery

Surgeries for weight loss can be classified as follows:

  • Restrictive procedures that limit the amount of food intake by reducing the size of the stomach
  • Malabsorptive procedures that interfere with absorption of food from the digestive tract
  • Combined restrictive and malabsorptive procedures

The 2 most commonly performed operations for weight loss in the United States are the Roux-en-Y gastric bypass (RYGB) and the adjustable gastric band (AGB). Both procedures could be done laparoscopically with smaller incisions than those required for traditional open approach (laparotomy). Small incisions result in less pain, early ambulation, and rapid postoperative recovery and less chance for wound complications (wound infection, fluid collection, and hernia).

Preoperative Workup

Careful preoperative patient screening, selection, preparation, and education are the keys for postoperative success. A comprehensive multidisciplinary approach to patients’ screening and education, including consultations with a dietitian, psychologist,internist, and bariatric surgeon is mandatory. In selected cases, cardiac, pulmonary, and endocrine evaluation may be needed. Patients should have a clear understanding and realistic expectation of benefits, risks, and long-term consequences of surgical treatment.

Operative Procedures

Gastric bypass

Roux-en-Y gastric bypass is the most commonly performed weight loss procedure in the United States. This operation both restricts food intake and limits absorption of food. A part of the stomach is closed off, creating a small pouch. This restricts the amount of food that you can eat at one time. The small pouch of the stomach is connected directly to the small bowel. As the name implies, food bypasses the stomach and the first portion of the small intestine. Because a part of the small bowel is bypassed, less food is absorbed.

Most people find they can eat less than 1 cup of food at a time after the operation. Food must be chewed very well. Overeating or not chewing food finely will result in cramping, nausea, and vomiting.

Laparoscopic adjustable gastric binding

This is a purely restrictive procedure. It involves placing an inflatable silastic band around the uppermost part of the stomach. This results in a smaller upper stomach pouch and a narrow opening between the upper and lower parts of the stomach. This induces and early feeling of fullness and thereby decreases food intake. It is adjustable by changing the volume of saline in a surgically placed subcutaneous reservoir, thereby tightening or loosening the band.

Biliopancreatic diversion

Biliopancreatic diversion (BPD) is a malabsorptive procedure with some restrictive component. A part of the stomach is removed and the remaining part is attached directly to the small intestine near its end. BPD is used much less often than Roux-en-Y because it has a greater risk of complications.

Vertical banded gastroplasty

Vertical banded gastroplasty (VBG, stomach stapling) is a restrictive procedure that traditionally was done by applying bands or staples to the stomach. This procedure is rarely performed today due to the high failure rate.

More information about these procedures can be obtained by visiting the American Society for Bariatric Surgery or the Bariatric Multidisciplinary Institute.

Benefits and Risks of Weight-Loss Surgery

Like all surgical procedures, weight-loss operations have benefits and risks. No one should decide to have surgery without being completely informed of both the pros and cons. This is a decision that you make with your family members, your health care provider, and your surgeon.

Benefits of weight-loss surgery

  • Weight loss: Most patients begin to lose weight right away. Some gain some of the weight back, but most are able to keep the weight off for long periods.
    • In general, combined restrictive and malabsorptive procedures (like gastric bypass) are more successful than restrictive procedures (like adjustable gastric banding) at promoting weight loss.
      • Gastric bypass is the most successful procedure. In the first 2 years after gastric bypass, average weight loss is 65% of excess weight. On the other hand, average weight loss with AGB is 35% of excess weight.
      • With gastric bypass, no band is introduced into the body. Also, it is a good operation for a sweet eater because eating sugar makes the patient feel ill (referred to as “dumping”).
      • The lap-band system has the advantages of being less invasive, providing a faster recovery, and avoiding alteration of anatomy of the gastrointestinal tract. It is adjustable and reversible with normal stomach restoration. No opening of the stomach or intestines occurs that could cause a leak.
    • People who undergo one of these procedures are much more likely to reach their goal and keep weight off if they also adopt a plan of healthy eating and regular exercise.
  • Improved health: Most obesity-related medical conditions improve drastically after surgery, especially diabetes, sleep apnea, and hypertension.
    • After surgery mortality rate is reduced and improvements are seen in many of the health risks associated with obesity.
    • Overall, quality of life, self image, and mobility are reported to be better.

Risks of weight-loss surgery

All surgical procedures have complications. Talk to your surgeons about this and make sure that your surgeons are specialists in bariatric surgery.

  • Disadvantages of gastric bypass – A patient who has gastric bypass may develop the following complications:
  • “Dumping syndrome” – Patients experience nausea, abdominal cramping, and diarrhea after eating sugar. Other symptoms include weakness or faintness.
    • Narrowing or ulcer formation or leak at the stomach to intestine connection – These may require reoperation.
    • Incisional hernia – This is more common in open bariatric surgery.
    • Blood clot in the leg – This may migrate to the lung.
    • In addition to surgical complications, long-term consequences of themalabsorption arise if patients with gastric bypass do not take supplemental vitamins, iron, and calcium. These nutritional deficiencies include the following:
      • Vitamin deficiencies (A, B-12, D, E, and K)  – Deficiencies of vitamin B-12, folate, and iron can cause anemia.
      • Mineral deficiencies (calcium, iron, and folic acid) – Calcium deficiency is a concern because it may lead to osteoporosis and other bone disorders.
  • Disadvantages of adjustable gastric band
    • The lap-band system is not the operation of choice in sweat eaters or patients with severe gastroesophageal reflux disease (GERD).
    • There is a low possibility of port leak or infection, as well as slippage,erosion, or migration of the band. This may require reoperation. High conversion rates of band to gastric bypass have been reported in American studies. However, this may represent the surgeon’s learning curve.

In experienced hands, the benefits of surgery are typically viewed to outweigh the risks. The immediate operative mortality rate for both adjustable gastric band and Roux-en-Y gastric bypass is about 1%.

Weight regain after bariatric surgery

Some patients may regain weight after bariatric surgery. This may be due to many factors, among them the following:

  • Noncompliance with postoperative diet
  • Noncompliance with postoperative exercise
  • Stretching of the stomach pouch
  • Communication between the pouch and the rest of the stomach
  • Band problems

Costs of weight loss surgery

Surgery seems to be much more expensive than other treatments for obesity; however, rates vary depending on choice of surgeon and hospital and region in which you live. Insurance coverage of weight-loss surgery varies by insurance carrier. Check with your carrier to see whether such operations are covered.

Postoperative Care

If you undergo weight loss surgery, you will continue to receive close medical care for the rest of your life. Laparoscopic adjustable gastric banding will require more frequent visits for band adjustment. Postoperative dietary (including vitamin, mineral, and possibly liquid protein supplementation), exercise, and lifestyle changes should be reinforced by counseling, support groups, and working with your primary care physician. Postoperative care may include planning for reconstructive operations after weight stabilization for certain patients.

For More Information

Web Links

MedlinePlus, Weight Loss Surgery
MedlinePlus, Obesity
American Obesity Association, Obesity Surgery

Adaptive Thermogenesis in resistant weight control Part II

Tuesday, October 12th, 2010

In our last article, we looked at adaptive thermogenesis as a cause of resistant weight control. Adaptive thermogenesis is energy expenditure to produce heat beyond that which is proportional to the amount of overfeeding associated with theoretical costs of an increased body size and a larger food intake. If there is no adaptive thermogenesis which is energy expenditure beyond that associated with overfeeding, then weight gain will be considerable.

We found that in clinical studies on overfeeding, there are differences between obesity prone and obesity resistant subjects and this could be due to the variances in such individuals in their adaptive thermogenesis. Those who are obese resistant tend to increase their energy expenditure with increased energy intake beyond the obligatory costs of the additional weight gain. {{{*}}}

It is interesting to note the effect of different nutrients in the overfeeding diet on fat storage. When digested foods enter the bloodstream there is an oxidative hierarchy. The macronutrient that is most easily stored (fat) is oxidized last, while macronutrients that cannot be stored at all (alcohol), or that can only be stored under certain circumstances (protein) or in limited amounts (carbohydrate) are oxidized first [1]. Alcohol ingestion directly increases alcohol oxidation, which is maintained until all alcohol is cleared. Protein and carbohydrate oxidation closely follow intake. In contrast, fat intake does not stimulate fat oxidation. Moreover, fat oxidation is inhibited by high intakes of the other macronutrients [1-3]. The thermic effect of the separate macronutrients is 20 to 30% for protein, 5 to 15% for carbohydrate, and 0–3% for fat [3]. The figure for the thermic effect of alcohol is not clear, values range between 6 and 30% in different studies [4]. Thus the type of nutrient intake could influence adaptive thermogenesis, protein being the most efficient.

The macronutrient composition of the diet can influence energy storage. With carbohydrate overfeeding 75 to 85% of the excess energy was stored and the remaining expended, while with fat overfeeding 90 to 95% of the excess energy was stored, but there was no difference in fat storage after 14 d between the two diets fed isoenergetically to the same subjects [5]. Lammert et al. [6] also found similar fat storage on high-carbohydrate and high-fat overfeeding. Overfeeding mixed diets resulted in a large variation in energy storage. The percentage of the excess energy intake that is stored ranged between 60 to 90% [7-11].

Adaptive Thermogenesis as a Protective Mechanism Against Environmental Hazards

The research conducted in Laval University during the past 10 years on body organochlorines (OCs) and obesity probably offers the best example to discuss the issue of a protective role for adaptive thermogenesis. As previously described, the interest for OCs in the study of obesity is related to their lipid soluble properties.[12] Despite the fact that the use of these compounds has now been banned in many countries for several decades, they persist in the body of every person on the planet because of their long half-life and their transport via air from countries where they still remain in use.[13-15] As summarized in Table 3 , their effects on thyroid function and mitochondrial functionality theoretically confer to these compounds an antithermogenic profile.

 Table 3. Potential Detrimental Effects of Organochlorines on Adaptive Thermogenesis

Effects Ref.
Decrease in thyroid hormone synthesis 16
Decrease in plasma T3 and T4 17-18
Increase in thyroid hormone clearance 19
Decrease in skeletal muscle oxidative potential 20
Inhibition in enzyme activities of the mitochondrial electron transport chain 21

At the end of the 1970s, Backman and Kolmodin-Hedman were the first investigators to report a significant increase in circulating OCs with body weight loss.[22] This hyperconcentration in plasma OCs depends on body weight loss, specifically, the importance of the decrease in their dilution space. In this regard, it was recently demonstrated that the increase in the plasma concentration of OCs corresponded to 388% of baseline values in obese patients tested 1 year after bariatric surgery.[23]

The integration of these observations also led some of us to examine the potential impact of OCs as an explanatory factor for the decrease in thermogenesis favored by weight loss in humans. Since this issue also cannot be directly tested for ethical reasons, a stepwise multiple regression analysis was used to quantify the contribution of various factors, including OCs, on the variance of changes in sleeping metabolic rate induced by body weight loss. The main finding of this study was that changes in plasma OC concentration explained half of the variance in the greater than predicted decrease in sleeping metabolic rate measured by whole-body indirect calorimetry.[24]

This finding is ecologically important since it provides an indication of the potential detrimental role of chemical pollution on the control of human energy expenditure. Since the documentation of this effect is the outcome of an association study rather than of a direct experimental demonstration, it is clear that it will not be possible to get a definitive proof of this concept. However, biological common sense would suggest that the accentuation of the thermogenic decrease occuring with weight loss appears to be useful to attenuate the decrease in the dilution space of OCs and to prevent more pronounced perturbations of body homeostasis.


The observations presented in this paper indicate that greater than predicted decrease in energy expenditure may happen in response to weight loss in obese individuals. The extent to which this may represent a thermogenic defect is debatable, but its ability to interfere with weight loss seems to be much clearer. Furthermore, this paper suggests that such a decrease would not occur randomly since it appears to be, at least partly, the consequence of fluctuations in body pollutants, which are known to produce detrimental effects on health and factors involved in the control of body thermogenesis.

Future Perspective

This paper provides evidence suggesting that equations estimating metabolic rate may not be adequate to determine energy needs in some individuals. This is likely the case for some obese individuals who are tested after weight loss when metabolic rate can be substantially lower than what is predicted by changes in body weight or composition. In this context, it is likely that the clinical evaluation of obese and weight-reduced individuals may require a greater level of sophistication by incorporating techniques such as indirect calorimetry in the evaluation setting. Without such an improvement in clinical characterization, the physiological vulnerability and the good compliance of some patients might remain unrecognized realities.

Executive Summary

  • This paper documents the clinical significance of adaptive thermogenesis that is defined here as a greater than predicted change in energy expenditure in response to changes in energy balance.
  • In some patients tested after a weight-reducing program, this excess decrease in energy expenditure may reach 1 MJ/day or even more.
  • This adaptation reduces the ability to tolerate a prescribed energy deficit and may compromise the success of a weight-reducing program.
  • This decrease in thermogenesis can also be viewed as a protective mechanism by preventing a substantial decrease in the dilution space of lipid soluble pollutants.


  1. Stubbs J, Raben A, Westerterp-Plantenga MS: Macronutrient metabolism and appetite. In Regulation of food intake and energy expenditure. Edited by: Westerterp-Plantenga MS, Steffens AB, Tremblay A. Milan , Edra; 1999:59-84
  2.  Westerterp KR, Wilson SAJ, Rolland V: Diet induced thermogenesis measured over 24h in a respiration chamber: effect of diet composition. Int J Obes 1999 , 23:287-292. 
  3.  Raben A, Agerholm-Larsen L, Flint A, Holst JJ, Astrup A: Meals with similar energy densities but rich in protein, fat, carbohydrate, or alcohol have different effects on energy expenditure and substrate metabolism but not on appetite and energy intake. Am J Clin Nutr 2003 , 77(1):91-100. 
  4. Suter PM, Jequier E, Schutz Y: Effect of ethanol on energy expenditure. Am J Physiol 1994 , 266(4 Pt 2):R1204-12
  5. Horton TJ, Drougas H, Brachey A, Reed GW, Peters JC, Hill JO: Fat and carbohydrate overfeeding in humans: different effects on energy storage. Am J Clin Nutr 1995 , 62(1):19-29.
  6. Lammert O, Grunnet N, Faber P, Schroll Bjørnsbo K, Dich J, Olesen Larsen L, Neese RA, Hellerstein MK, Quistorff B: Effects of isoenergetic overfeeding of either carbohydrate or fat in young men. Brit J Nutr 2000 , 84:233-245.
  7. Tremblay A, Despres JP, Theriault G, Fournier G, Bouchard C: Overfeeding and energy expenditure in humans. Am J Clin Nutr 1992 , 56:857-862  
  8. Ravussin E, Schutz Y, Acheson KJ, Dusmet M, Bourquin L, Jequier E: Short-term, mixed-diet overfeeding in man: no evidence for “luxuskonsumption”. Am J Physiol 1985 , 249(5 Pt 1):E470-7
  9.  Roberts SB, Young VR, Fuss P, Fiatarone MA, Richard B, Rasmussen H, Wagner D, Joseph L, Holehouse E, Evans WJ: Energy expenditure and subsequent nutrient intakes in overfed young men. Am J Physiol 1990 , 259(3 Pt 2):R461-9. 
  10. Bouchard C, Tremblay A, Despres JP, Nadeau A, Lupien PJ, Theriault G, Dussault J, Moorjani S, Pinault S, Fournier G: The response to long-term overfeeding in identical twins. N Engl J Med 1990 , 322(21):1477-1482.
  11.  Norgan NG, Durnin JV: The effect of 6 weeks of overfeeding on the body weight, body composition, and energy metabolism of young men. Am J Clin Nutr 1980 , 33(5):978-988
  12. Chevrier J, Dewailly E, Ayotte P, Mauriege P, Despres JP, Tremblay A: Body weight loss increases plasma and adipose tissue concentrations of potentially toxic pollutants in obese individuals. Int. J. Obes. Relat. Metab. Disord.24(10), 1272-1278 (2000).
  13. Barrie LA, Gregor D, Hargrave B et al.: Arctic contaminants: sources, occurrence and pathways. Sci. Total Environ.122(1-2), 1-74 (1992).
  14. Iwata H, Tanaba S, Sakal N, Tatsukawa R: Distribution of persistent organochlorines in the oceanic air and surface seawater and the role of ocean in their global transport and fate. Environ. Sci. Technol. 27, 1080-1098 (1993).
  15. Ma J, Daggupaty S, Harner T, Li Y: Impacts of lindane usage in the Canadian prairies on the Great Lakes ecosystem. 1. Coupled atmospheric transport model and modeled concentrations in air and soil. Environ. Sci. Technol. 37(17), 3774-3781 (2003).
  16. Collins WT Jr, Capen CC, Kasza L, Carter C, Dailey RE: Effect of polychlorinated biphenyl (PCB) on the thyroid gland of rats. Ultrastructural and biochemical investigations. Am. J. Pathol. 89(1), 119-136 (1977).
  17. Koopman-Esseboom C, Morse DC, Weisglas-Kuperus N et al.: Effects of dioxins and polychlorinated biphenyls on thyroid hormone status of pregnant women and their infants. Pediatr. Res. 36(4), 468-473 (1994).
  18. Hagmar L, Rylander L, Dyremark E, Klasson-Wehler E, Erfurth EM: Plasma concentrations of persistent organochlorines in relation to thyrotropin and thyroid hormone levels in women. Int. Arch. Occup. Environ. Health 74(3), 184-188 (2001).
  19. Barter RA, Klaassen CD: Reduction of thyroid hormone levels and alteration of thyroid function by four representative UDP-glucuronosyltransferase inducers in rats. Toxicol. Appl. Pharmacol. 128(1), 9-17 (1994).
  20. Imbeault P, Tremblay A, Simoneau JA, Joanisse DR: Weight loss-induced rise in plasma pollutant is associated with reduced skeletal muscle oxidative capacity. Am. J. Physiol. Endocrinol. Metab. 282(3), E574-E579 (2002).
  21. Pardini RS: Polychlorinated biphenyls (PCB): effect on mitochondrial enzyme systems. Bull. Environ. Contam. Toxicol.6(6), 539-545 (1971).
  22. Pelletier C, Imbeault P, Tremblay A: Energy balance and pollution by organochlorines and polychlorinated biphenyls.Obes. Rev. 4(1), 17-24 (2003).
  23. Hue O, Marcotte J, Berrigan F et al.: Increased plasma levels of toxic pollutants accompanying weight loss induced by hypocaloric diet or by bariatric surgery. Obes. Surg. 16(9), 1145-1154 (2006).
  24. Tremblay A, Pelletier C, Doucet E, Imbeault P: Thermogenesis and weight loss in obese individuals: a primary association with organochlorine pollution. Int. J. Obes. Relat. Metab. Disord. 28(7), 936-939 (2004).


Tuesday, September 28th, 2010

Wonder why it is so difficult for some of your patients to lose weight? There have been many studies that documented substantial reduction in calorie diet intake of some patients and yet their weight remains the same.  We have covered some of the undetected hypothyroidism and leptin resistance as causes. However, there is another interesting study on the effect of adaptive thermogenesis on resistant weight control. The hypothesis is that the body has an adaptive mechanism in thermogenesis to balance energy expenditure. When dietary intake is down or energy expenditure is up, the body decreases its thermogenesis to maintain weight. Many well-designed studies have demonstrated some thermogenic deficit or related physiological vulnerability in individuals predisposed to obesity.{{{*}}}

In a study by Tremblay et al from Canada, the authors defined Adaptive thermogenesis as the decrease in energy expenditure beyond what could be predicted from body weight or its components (fat-free mass and fat mass) under conditions of standardized physical activity in response to a decrease in energy intake. As expected, energy expenditure, be it in the resting or the active state, was significantly more decreased compared with what was predicted by morphological changes. In addition, the authors recently reported the maximal decrease in resting energy expenditure in this study, which was sufficient to completely compensate for the prescribed energy deficit.

Body weight instability, which is also generally referred to as the ‘yoyo phenomenon’, seems to be the normal biological reaction to uncontrolled and quantitatively important negative energy balance. The weight regain that generally follows this large energy deficit may exceed weight loss so that a net weight gain may be the outcome of such a weight cycle. . Approximately two decades ago, the yoyo effect was tested as a factor that could explain, per se, the proneness to a positive energy balance in animals.

The authors had the opportunity to complete two case studies in which they could test the effect of weight cycling on adaptive thermogenesis under well-standardized conditions. In the first study, an athletic male explorer was first tested in the Laval University respiratory chamber under well-standardized experimental conditions. As shown in Figure 1, this measurement was followed by pre-expedition overfeeding that induced a 5 kg weight gain. After overfeeding, he engaged in a 22-day cross-country skiing expedition through Greenland that resulted in a weight loss of 8.5 kg. Figure 1 also shows that indirect calorimetry measurements were repeated after he had recovered his baseline morphological profile. It is also important to note that this post-expedition measurement was performed under conditions similar to baseline measurement for energy and macronutrient intake, as well as for spontaneous physical activity in the chamber. Despite this optimal standardization for factors influencing ‘obligatory thermogenesis’, daily energy expenditure was reduced by 1.4 MJ (approximately 350 kcal) following the expedition.

Figure 1.  Variations in body weight and daily energy expenditure in response to a weight cycle imposed by an expedition in Greenland (Subject 1) and in Antarctica (Subject 2).

A comparable result was obtained in the second study, which involved the testing of another male explorer who was also subjected to whole-body indirect calorimetry measurements before and after a 65-day expedition in Antarctica. As expected, the expedition induced a considerable body weight loss (13.2 kg) that had to be recovered following the expedition before a second series of measurements could be performed in the respiratory chamber. Thus, as for case study 1, this subject was tested at the same body weight and composition status before and after the expedition as well as under standardized nutritional and activity conditions in the chamber. Figure 1 shows that the weight loss/regain cycle again resulted in a marked decrease (1.0 MJ/day) in daily energy expenditure, which provides further evidence of the impact of weight cycling on adaptive thermogenesis.

The main implication that can be derived from the observations presented above is that adaptive thermogenesis can be sufficiently pronounced in some individuals to interfere with successful weight loss. On the basis of the studies of Leibel et al.and those performed in Laval University, this phenomenon could appear as an adaptation that promotes the early occurrence of resistance to lose fat. Indeed, in these two series of studies, greater than predicted decreases in energy expenditure were observed in subjects having experienced some weight loss.

The authors’ clinical experience also reveals that such an adaptation can happen sufficiently early during the course of a weight-reducing program to totally prevent the achievement of weight loss

In summary, there seem to be some obese individuals who clearly overreact in energy expenditure when they are exposed to a negative energy balance. This adaptive thermogenesis may then clearly reduce the ability to achieve a successful body weight loss. To date, there is no clear explanation for the occurrence of such a phenomenon but, as discussed in the next posting, the authors proposed a the possibility that it might happen so as to protect body homeostasis due against the influence of environmental pollutants.

Undiagnosed hypothyroidism the cause of difficulty in weight loss?

Monday, September 13th, 2010

Some women have trouble losing weight because of a hormonal problem. The thyroid gland, located in the neck, pumps out hormones that control body metabolism. If the gland’s output isn’t high enough, a condition known as hypothyroidism, the pounds can pile on – and stay on.
Oprah Winfery is just one of many celebrities to suffer from hypothyroidism. She wrote that the condition “slowed down my metabolism and made me want to sleep all the time. (Most people gain weight. I did! Twenty pounds!)”
According to the American Association of Clinical Endocrinologist, more than 27 million Americans suffer from thyroid dysfunction, half of whom go undiagnosed. Of the detected cases of hypothyroidism, more than half are due to an autoimmune disorder called Hashimoto’s disease, in which the immune system attacks and destroys thyroid gland tissue. Many patients with hypothyroidism are ignored by health care practitioners due to the vague symptoms they present or that their lab tests conducted by conventional laboratories are normal. Such vague hypothyroid symptoms losing hair, constipation, sluggishness, fatigue, mental fogginess, and inability to lose weight. Often, thyroid test includes TSH and total tyrosine (inactive T4), most labs are not able to assay T3 (the only active form of thyroid hormone) and reverse T3 (inactive form). Therefore, it is not unusual for your doctors to consider you as normal. Sometimes, the only clue is a slightly raised TSH.

Dr Datis Kharrazian wrote an excellent book on “Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal” In the book, the author states that irregular immune function, poor blood sugar metabolism, gut infection, adrenal issue, and hormonal imbalance  can all significantly depress thyroid function.  Sometimes, physicians would prescribe thyroid hormones. While prescription thyroid hormones might bring their levels in the blood to a normal range, the hormone replacement doesn’t address what caused the thyroid to falter in the first place. In this book, author lays out a plan to address many different forms of thyroid diseases, and not only hypo/hyper thyroidism and I would highly recommend this to anyone who has an interest in helping the many subclinical hypothyroid patients who are living in sub optimal health.

Hypothyroidism occurs when the thyroid is consistently underactive for a variety of reasons. The author states that autoimmune Hashimoto’s disease is the most common cause of hypothyroidism.Because Hashimoto’s is an immune disease, it often goes undiagnosed and is largely mismanaged by both conventional and alternative health care system. People with Hashimoto’s often don’t respond well to thyroid replacement hormones according to the author. A TPO and TGB serum antibody test helps identify Hashimoto’s. A negative test is sometimes false as the immune system fluctuates. Symptoms such as heart palpitation, trembling, increased pulse rate, insomnia, night sweats, feeling cold, tired, depression, losing hair strongly suggest the disease, repeat tests should be done to confirm the diagnosis. With Hashimoto’s, typical treatment of iodine for goiter will exacerbate this condition so iodine has to be avoided. Numerous studies have shown a link between gluten intolerance and Hashimoto’s. If the patient have Hashimoto’s, eating a gluten-free diet, avoiding wheat and wheat-like grains such as barley, rye, spelt, triticale, kamut, and oats is helpful. The gluten molecule is very similar to the thyroid gland molecule, and antibodies developed against the gluten protein will attack the thyroid glands. There are some risk factors for developing Hashimoto’s such as gluten intolerance, insulin resistance, PCOS (polycystic ovary syndrome), estrogen fluctuation, vitamin D deficiency, chronic infection, inflammation, or an immune reaction to heavy metal or environmental pollutant.

We don’t always know what triggers an autoimmune disease, although compromised immune barrier in the digestive tract is often a factor. When the gut lining loses integrity due to poor diet, infections, blood glucose swings, and adrenal malfunctions, the immune system is constantly on call. This leads to immune system imbalance and the development of an autoimmune disease. The majority of people with hypothyroidism do not need thyroid hormone medications. The author believes that replacement thyroid hormones could make functional hypothyroidism irreversible. This author breaks down functional hypothyroidism into six patterns.

1.      Primary hypothyroidism – true dysfunction of the thyroid gland, and is the only pattern of hypothyroidism that can be effectively managed with replacement hormone, unless it’s autoimmune Hashimoto’s.

2.      Hypothyroidism secondary to pituitary hypofunction – this is very common pattern of functional hypothyroidism. TSH will be low (below 1.8), although not as low as with hyperthyroidism, and the person will have symptoms of an underactive thyroid.

3.      Thyroid under-conversion – this is a common pattern associated with chronic adrenal stress and excess production of the adrenal hormone cortisol. In this case body makes plenty of T4, but too much cortisol prevents the body from being able to convert enough T4 and T3, the form of thyroid hormone the body can use. An elevated cortisol level suppresses the conversion of T4 to the useable T3. Selenium and iron are also essential elements in this conversion.

4.      Thyroid over-conversion and decreased TBG – elevated levels of testosterone in women create this pattern of too much T4 being converted to T3, and underproduction of thyroid binding globulin(TBG). The excess T3 overwhelms the cells so they develop a resistance to the thyroid hormone and it can’t get into the cells, As a result, the person with this disorder has hypothyroid symptoms.

5.      Thyroid binging globulin elevation – this pattern is often associated with oral contraceptive or estrogen replacement therapy. When estrogen levels are too high, as often happens in women taking birth control pills, or hormone replacement therapy, the body makes too much TBG. Since thyroid hormones in the bloodstream bind to the excess TBGs, not enough free hormones are available to enter the cells. In people with this pattern, clearing the body of excess estrogen address hypothyroidism.

6.      Thyroid resistance – this is another stress-related pattern in which the pituitary and thyroid glands function normally and make the right amount of thyroid hormones, but the hormones are not getting into the cells to take effect. In this case, managing adrenal health is the treatment.

This author also stressed that control anemia is very important for hypothyroid patients. It should be always addressed first. He states that when anemia doesn’t respond to iron supplementation, it is often a result of chronic inflammation and managing that problem often resolves the anemia. One other major concern that has to be address with hypothyroidism is dysglycemia. Not able to control hypo-or hyper-glycemia with patients will interfere with the treatment of hypothyroidism. The disease hypothyroidism is of concern for all ages, from cradle to grave. In this book, the author suggests that autoimmune disease of the mother is often the root cause of autism, with the immune system attacking the brain or nerve tissue of the child with autism. Children born with an hyperactive immune system is a ticking bomb and are vulnerable to any foreign particles particularly proteins that can trigger a violent autoimmune attack to any vital organs in the body . These xenobiotics include vaccines, food intolerance and heavy metal toxicity aggravated by blood sugar and hormonal imbalance. The author also highlighted the fact that nutrients could play a critical role in regulating thyroid functions through its influence on the factors that drive functional hypothyroidism. Eating nutrient rich diet could address  dysglycemia, anemia, infections, leaky gut syndromes, and adrenal stress that underlie most  thyroid problems.

Thus with the right diagnosis, measuring T3 and reverse T3 and the right dietary approach, common thyroid problems especially the frequently missed hypothyroidism could be resolved. This is especially important in patients with resistant weight management and it might be surprising to find that functional hypothyroidism could be a major contributing factor to your difficulty in losing weight.

Obesity – genes or diet?

Tuesday, August 24th, 2010

Obesity – nature or nurture….genetic factors are at play in obesity. But you are not doomed by your genetic fate…nutrients have been demonstrated to regulate your fat genes..{{{*}}}

There is a constant debate over the causative factors of obesity. Are diet and lifestyle habits more important than genetic predisposition. I must say that these factors are not mutually exclusive. Dean Ornish and his colleagues have demonstrated that while genetic predisposition might handicap and put certain population segments at higher risk, dietary intervention do have tremendous influence on gene regulation even in a very short period of time.  In May 2008, he and his colleagues published an article in the Proceedings of the National Academy of Sciences that after only 3 months of making lifestyle and nutritional changes, gene expression in over 500 genes was beneficially affected – upregulating disease-preventing genes and downregulating disease promoting genes including oncogenes involved in prostate cancer(1).

The purist of the dieting influence is of the view that obesity is entirely due to bad dietary behaviour. Dr David Heber (Director, UCLA Center for Human Nutrition) is a proponent of that view. He said, “Genes load the gun, but environment pulls the trigger. The idea that it’s all in your genes is nonsense. The human genome changes only one half of one percent every million years. The obesity epidemic is only about 30 years old, so changes in genes do not explain the recent dramatic rise in obesity, not only in this country but also worldwide”.

However, small gene variations called SNPs or single-nucleotide polymorphisms are much more common than major gene changes that happen only over millions of years. Such polymorphisms could affect huge populations that could account for their role in obesity and risk factors such as hypercholesterolemia. In a recent study, researchers at the University of Oxford found in 13 cohorts of 38,759 participants, approximately 50 percent of white Europeans have one defective copy of the FTO gene which increased the risk of obesity by about one third, while 16 per cent of people have two altered copies of the gene have a 70 percent increased risk of obesity(2). The FTO gene expression was also found to be significantly upregulated in the hypothalamus of rats after food deprivation and expressed in the neurons of feeding-related nuclei of the brain. Increases in hypothalamic expression of FTO are associated with the regulation of energy intake but not feeding reward.

A recent study by investigators in Finland(3) randomly assigned men and women with metabolic syndrome to a rye-pasta diet (low glycemic index) or an oat-wheat-potato diet (high glycemic index). After only 12 weeks, those in the low glycemic index LGI group had 71 genes showing decrease expression and none showing increased expression. In the high glycemic index group, 62 genes showed increased expression and none showed decreased expression. Two specific genes that were down regulated in the LGI  are particularly important. HSL (hormone sensitive lipase), a key enzyme in the release of fatty acids from adipose tissue and stimulation of insulin are downregulated in the LGI group. The other important transcription factor, TCF7L2 is the strongest known predictor of type 2 diabetes. This factor occurs with increased frequency in individuals with type 2 diabetes.

The editorial that accompanies this article is really pertinent “Molecular pathways involved in hormone action have been the target of multibillion-dollar pharmaceutical research effort. However, many of these pathways, may normally be under dietary regulation. The results of the present study emphasize the age-old wisdom to “use food as medicine” – in this case, for the targeted prevention and treatment of obesity, diabetes and heart diseases.

This has great relevance in the area of nutrigenomics. Your genes especially bad genes need not seal your destiny, many of the molecular pathways dictated by such genes could be regulated by simple inexpensive dietary interventions that need not be protracted as well. Herein lies the mystery of the gene and dietary interactions that is driving the debate in our current thread.


  1. Dean Ornish, Mark Jesus M. Magbanua, Gerdi Weidner, Vivian Weinberg, Colleen Kemp, Christopher Green, Michael D. Mattie, Ruth Marlin, Jeff Simko, Katsuto Shinohara,Christopher M. Haqq, and Peter R. Carroll Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention Proceedings of the National Academy of Sciences June 17, 2008 vol. 105 no. 24 8369-8374
  2. Frayling, N. Timpson, M. Weedon, et al. 2007. A common variant in the FTO gene is associated with body mass index and presidsposes to childohood and adult obesity. Sciewnce 316 (5826):889-94
  3. Salsberg S.L and D. S Ludwig, 2007 putting your genes on a diet: The molecular effects of carbohydrate. Am J Clin Nutr 85(5): 1169-70.

Waist Circumference, an independent risk factor

Saturday, August 21st, 2010

Waist circumference (WC) is a risk factor for mortality in older adults, regardless of body mass index  (BMI), according to the results of a large US cohort study reported in the August 9/23 issue of the Archives of Internal Medicine. Using the Cancer Prevention Study II Nutrition Cohort, the investigators evaluated the association between WC and mortality among 48,500 men and 56,343 women, aged at least 50 years. Between 1997 and the end of follow-up in 2006, there were 9315 deaths in men and 5332 in women.{{{*}}}

Risk for mortality was more than doubled for very high levels of WC after adjustment for BMI and other risk factors. Among men, relative risk (RR) of mortality was 2.02 (95% confidence interval [CI], 1.71 – 2.39) for WC 120 cm or larger compared with WC less than 90 cm. Among women, RR was 2.36 (95% CI, 1.98 – 2.82) for WC 110 cm or larger compared with WC less than 75 cm.

Within all categories of BMI, WC was positively associated with mortality. A 10-cm increase in WC in men was associated with RRs of 1.16 (95% CI, 1.09 – 1.23) for normal (BMI, 18.5 kg/m2 to <25 kg/m2), 1.18 (95% CI, 1.12 – 1.24) for overweight (BMI, 25 kg/m2to <30 kg/m2), and 1.21 (95% CI, 1.13 – 1.30) for obese (BMI, ?30 kg/m2) BMI. For women, RRs were 1.25 (95% CI, 1.18 – 1.32), 1.15 (95% CI, 1.08 – 1.22), and 1.13 (95% CI, 1.06 – 1.20), respectively

The waist circumference is perhaps the best index of visceral fats. These fat cells are no longer considered as passive storage of fats but are actively secreting cytokines such as TNF? that could affect insulin resistance , and PAI-1, a cytokine that could lead to thrombosis and inflammation . It has been demonstrated that hyperinsulinemia was positively linked to adipose TNF- and IL-6 gene expression, and hyperinsulinemia and glucose intolerance were negatively linked to adipose adiponectin expression. The latter hormone together with leptin regulate satiety and therefore are important in weight control. These 2 cytokines are known to be secreted mainly by subcutaneous fat. However, a study shows that central obesity with visceral fats reduce the secretion of these cytokines and are associated with obesity. It is also shown that obese patients eventually develop leptin resistance and are not able to control eating due to the loss of signals to the brain on satiety.

Can gut bacteria cause obesity?

Thursday, June 10th, 2010

Recently, there has been considerable interest in the role of gut bacteria and weight control. Could bacteria in the gut play a role in obesity just as helicobacter plays a role in stomach cancer? This post reviews the latest studies on this subject. The gut bacteria have been shown to impact insulin resistance, inflammation, and adiposity via interactions with epithelial and endocrine cells.

Up until the last few decades, obesity has been a rare physiological state. Now obesity as defined by BMI of more than 30 is reaching a global epidemic. Globesity is an appropriate word for this global public health issue. The incidence of childhood obesity in China is rising and if not check, will lead to an explosion in obesity related chronic diseases in the future. The human body is a complex system, made all the more complex through its interactions with the trillions of microorganisms that coat the body surface and densely populate the gut.

Recent work has shown that the microbes of the gut may play a role in human metabolism and adiposity. Because they are environmentally acquired, microbes constitute one part of our environment that may contribute to the obese state.

This review by Dr Ruth E. Ley was posted on 18 Jan 2010 in the journal of Current Opinion of Gastroenterology. 2010;26(1):5-11.discusses the most recent findings and insights into the relationship between the human microbiota, obesity, and obesity-associated diseases.

Patterns of Microbial Diversity in Relation to Obesity

The initial link between gut microbial ecology and obesity was made in leptin-deficient mice (mice homozygous for an aberrant leptin gene, ob/ob) by Ley et al. Results from a 16S rRNA gene sequence survey revealed that the bacterial communities in the ceca of ob/ob mice had a different proportion of bacteria belonging to the two dominant phyla when compared with those of lean wild-type (+/+) or heterozygous (ob/+) mice, with a greater representation of Firmicutes and fewer Bacteroidetes characterizing the obese host microbiota. A subsequent metagenomic analysis of these same microbial communities, which was based on shotgun sequencing of the microbial community DNA, showed an enrichment in genes involved in energy extraction from food in the obese host’s microbiome relative to that of the lean host’s microbiome. A microbiota with greater energy extraction efficiency resulted in less energy left over in feces and greater levels of short-chain fatty acids (SCFAs) in the cecum. Furthermore, when the luminal contents from the ceca of obese or lean mice were provided to lean germ-free recipients, the mice receiving the microbes from the obese donors gained more weight over a 2-week period than recipients of the lean microbes, despite equivalent food intake. In a study extending these observations to humans, 12 obese participants were randomly assigned to either carbohydrate-restricted or fat-restricted diets, and on average, the proportion of Bacteroidetes bacteria enumerated via 16S rRNA gene sequencing increased over time, mirroring reductions in host weight but not changes in diet. Together these studies showed that the gut microbiota was generally altered in the obese host and could contribute to host adiposity in humans and mice.

Metagenomics and Obesity

A subsequent and much larger study of the microbiome associated with obesity conducted with humans also showed that obesity was associated with a depletion of Bacteroidetes, together with an enrichment in carbohydrate and lipid utilizing genes in the microbiome as a whole. Turnbaugh et al. focused on twins to assess the gut microbiota’s relationship to host weight. The fecal microbial communities of young adult female monozygotic (n = 31) and dizygotic (n= 23) twin pairs concordant for either leanness or obesity were compared, along with those of their mothers (n = 46), using a combination of traditional 16S rRNA gene clone libraries and high-throughput metagenomic analyses of the microbiome.

Fecal samples were obtained from the majority of participants at an initial time point and then again 2 months later. Comparisons between all 154 participants showed obesity to be associated with reduced bacterial diversity and reduced representation of the Bacteroidetes. Furthermore, the microbiome differed between obese and lean hosts in much the same way it had in the obese mouse model, with obese host microbiomes enriched in gene categories involved in carbohydrate and lipid metabolism.

Varied Patterns of Microbial Ecology in Relation to Weight

This and other patterns of fecal microbial ecology in relation to body weight in humans have been reported recently, and these are summarized in Table 1 . In studies that examine the effect of weight loss on the abundance of Bacteroides-related taxa, the relationship has been reported as positive, neutral, and negative. It is noteworthy that rather than using broad 16S rRNA gene surveys or metagenomics to assess the composition of microbial communities, these studies enumerated specific taxa using probes, which can differ between studies. Thus, the varying patterns of association between microbial taxa and host weight raise the question of how much impact the differences in methodology can have on the patterns observed. Biases are inherent to all of the methods employed in studies of microbial ecology, and the degree of bias can vary between samples within a study. This argues for better designed prospective studies in the future that will address variability of sampling and test methodologies. Be that as it may, the following studies do point the strong influence of gut bacteria on body weight.

Table 1. Human studies of gut microbial ecology in relation to body weight

Author Participants Method (sample type) Finding
Ley et al. 12 obese participants on one of two diets, carbohydrate or fat-reduced, for 1 year; two lean controls 16S rRNA surveys by Sanger sequencing (feces) Proportion of Bacteroidetes sequences increased over time, on average, and correlated with weight loss. No difference between diets
Turnbaugh et al. 154 participants, MZ and DZ twins and mothers, obese or lean 16S by Sanger and 454 pyrosequencing, metagenomics (feces) Reduced levels of diversity, and reduced levels of Bacteroidetes in obese participants; metagenomes of obese participants enriched in energy harvesting genes
Schwiertz et al. 30 lean, 35 overweight, 33 obese participants qPCR for Bacteroidetes, Actinobacteria, Archaea (feces) More Bacteroidetes in overweight and obese vs.lean participants, and more Methanobrevibacter in lean participants
Collado et al.[ Women before and during pregnancy, 18 overweight participants and 36 controls FISH/flow cytometry and qPCR (feces) Higher levels of Bacteroidetes and S. aureus in overweight, positive correlation between Bacteroides levels and weight gain over pregnancy
Sotos et al. 8 obese and overweight adolescents during weight loss FISH (feces) Enterobacteriaceae and sulfate-reducing bacteria reduced in group with greatest weight loss.Reduced levels of RoseburiaEubacterium in those with less weight loss
Duncan et al. Participants on weight loss diets over 8 weeks vs. Weight maintenance FISH counts (feces) No difference in Bacteroidetes levels between groups; reduced levels of Roseburia and Eubacterium, and increased levels of Clostridium spp., correlate with reduced carbohydrate intake
Kalliomaki et al. Obese and overweight children (n=25) and normal weight children (n=24); prospective study qRT-PCR and FISH/flow cytometry (feces) Children remaining lean at age 7 had higher levels of Bifidobacteria and lower levels of S. aureus, as infants
Santacruz et al. 36 adolescents on diet and physical activity, 10 weeks qPCR (feces) Bacteroides fragilis abundance correlated with carbohydrate intake. Levels of Bacteroides and Lactobacillus increased with weight loss
Nadal et al. 39 adolescents on diet and physical activity,10 weeks qPCR (feces) Clostridium histolyticum and E. rectaleC.coccoides reduced with weight gain; increase in BacteroidesPrevotella in high weight loss group
Sabate et al. 137 obese patients, 40 healthy controls Glucose-hydrogen breath test (for H2) and liver biopsy (breath, liver) Bacterial overgrowth in small intestine more common in obese vs. lean participants
Zhang et al. 3 lean, three obese, and three postgastric bypass participants Sanger and 454 sequencing of 16S rDNAs, qPCR (feces) Firmicutes more abundant in lean participants, lowest after gastric bypass. Gamma-Proteobacteria and Verrucomicrobia enriched after gastric bypass; higher Archaea in obese participants; overall communities of gastric bypass and obese participants more similar to each other than to lean participants

DZ, dizygotic; FISH, fluorescent in-situ hybridization; MZ, monozygotic.

Animal vs. Human Studies

In contrast to studies performed in humans, studies of gut microbial ecology and obesity conducted in animals tend to have less variable outcomes. Studies in rats and pigs have reported greater abundances of Bacteroidetes associated with the lean state, as observed in ob/ob mice. In a systems-biology approach, Waldram et al. studied a rat model of obesity, characterizing gut microbiotas in parallel with metabolites. Results broadly support patterns of greater Firmicutes/Bacteroidetes ratios observed in other animal studies. In addition, specific bacteria were associated with the obese phenotype (Halomonas and Sphingomonas), as were lower total bacterial counts and lower Bifodobacterial counts; furthermore, differences in microbial community composition correlated with differences in metabotypes.

Is the variation in outcomes of human studies related to the complexity of the human lifestyle? In animal studies, diet can be controlled precisely – this precludes any potentially modulating effects of variations in diet between participants e.g. where specific microbial taxa respond to changes in a diet’s content of specific carbohydrates. Yet, average human diets that are not designed for weight loss may add noise to data rather than skew results one way or another. Indeed, in a comparison of human vegetarians and omnivores allowed to eat their normal diet, Tap et al. did not note any major differences between gut microbiotas for the two diet groups. Rather than the composition of the diet, another factor that may be important to consider is how the food is ingested throughout the day, for instance, how long the fasting periods last. Fasted mice have been shown to harbor a greater proportion of Bacteroidetes in their ceca compared with unfasted mice with equivalent body fat. Thus, the frequency with which food enters the bowel and its transit time may be important factors to control for, or at least note, when comparing studies in humans.

Prospective Studies

The question of whether or not a microbial community can predispose a host to weight gain or loss has been addressed in animal models and human studies. One approach to this question has been to control the composition of the initial microbial community directly. This is accomplished by administering whole microbiotas of known composition by oral
gavage straight into the stomach of germ-free (usually mouse) recipients housed in asceptic isolators. As mentioned above, the result of such ‘transplantation’ of the gut microbes from obese (genetic or diet-induced models) to lean germ-free recipient mice is greater weight gain for mice that received obese-microbiotas. Although these transplantation experiments are h ighly artificial, they show that a microbiota can predispose the host to greater weight gain, and recent studies have shown these findings to be relevant to human health. Kalliomaki et al. Compared groups of children over time and observed that those who became overweight by age 7 had had lower levels of Bifidobacteria and higher levels of Staphylococcus aureus as infants compared with those that kept a healthy weight.

These researchers had banked samples over time and were able to go back to interrogate the microbiota of the same individuals prospectively. In shorter-term study, Santacruz et al.found that the response of overweight adolescents to a diet and exercise weight-loss program was dependent on the initial microbiota prior to the treatment. Both of these studies demonstrate that the microbiota are differentiated between people prior to the change in weight, which suggests that therapeutic interventions aimed at reshaping the gut microbiota may be beneficial for weight loss as well as preventive against weight gain.

Other Body Habitats

Clearly, obesity can be associated with a dysbiosis of the microbiota from the lower intestinal tract; recently, researchers have extended this observation to other parts of the body. In a study of the oral microbiota, Goodson et al  show differences in the diversity and abundances of salivary bacteria between overweight and healthy weight people.
Specifically, they found that Prevotellas (a group within the Bacteroidetes phylum) were in greater abundance in the overweight and Selenomonas was present only in the overweight individuals, suggesting that these taxa could be biomarkers for excess adiposity. Traveling further down the gastrointestinal tract, bacterial overgrowth in the small intestine has been shown to be more common in morbidly obese patients than in healthy weight individuals.Although  preliminary, these studies indicate that obesity may be associated with a dysbiosis of the normal microbiota throughout the body.

Mechanisms Linking the Microbiota to Obesity

Obesity is associated with a number of chronic conditions, including inflammation, insulin resistance, type II diabetes, hepatic steatosis, and cardiovascular disease. A number of recent studies have focused on the mechanistic links between gut microbes and specific conditions associated with obesity. Combining studies of host-microbial interactions relevant to obesity with studies of microbial diversity should lead to a more comprehensive understanding of which microbes, or microbial products, are the best targets for interventions
(such as pharmaceutical mimicry) aimed at improving health, aiding weight loss, or preventing weight gain.

In the next posting, we will discuss how the gut bacteria could mediate weight control through their effects on metabolism, inflammation, insulin resistance and the endocrine system.


Thursday, May 20th, 2010

Got your attention with that headline didn’t it? HOWEVER no guarantees that you can keep off the weight you have lost though, also no guarantees that it won’t adversely affect your health too!!

Yes, quick fix weight loss methods that “works” with minimal effort! These come in various forms like “magic” pills and “revolutionary” shakes to replace your daily food. Do they work? Yes for most of them, IF only weight loss you are after and IF you don’t care about the accompanying dangers to other aspects of your health, adverse effects or sustainability.

Before you succumb to the seduction of “minimal effort weight loss” you really need to understand how these methods “work” and the dangers that come with them – even when money is not an issue, it may be too high a price to pay in terms of your overall health and well being!

In truth, there isn’t a magic pill or potion that will get you healthily slim as would a sensible, comprehensive healthy lifestyle of exercise, balanced diet and rest.

Before we look at some of these “magic” solutions to weight loss, understanding how they work and the dangers which accompany each of them, let’s look at the equation and some notes on weight gain/loss;  Here’s my take on some of the weight management issue.

Weight Gain/Loss = Calorie intake – Calorie Output

Calorie intake comes from the food we consume each day; Calorie output comes with exercise, daily activities and metabolism in the body even at rest; the body converts the extra calories and stores them in the fat cells for future energy use.

Very very roughly, burning about 10,000Kcal of energy would burn off 1kg of fats. An adult leading a sedentary lifestyle with little to no exercise would roughly require about 3,000 Kcals a day. Jogging at about 8Kmph for 30 mins would burn about 300kcals. That’s hard work. These are only very rough guidelines.

So, with most of the minimal effort weight loss methods,there  is little to no extra exercise or muscle toning  but gimmicky tricks which interfere with food absorption eg fat blockers, make you not feel hungry – appetite suppressants – toying with your hormones and neurotransmitters eg  Leptin, Ghrelin , Serotonin etc, meal replacements – fill your tummy with very low calorie diet; and on the other side of the equation – increase your metabolic rate with stimulants which increases heart rate and other metabolic activity eg caffeine .


This usually contains a pharmacological agent called ‘orlistat’. This works by reducing about 30% of the absorption of dietary fat ie fat from the food you consume. Users claim to have lost up to 5kg in the 1st month and 7kg by the end of 3 months. Sounds good doesn’t it? But, there is a long list of side effects, some of which could be serious to you depending on your current condition. These side effects include loose, oily fatty stools, uncontrolled bowel movement and flatulence with discharge– all similar to those with a fat absorption/digestion condition. What can be perhaps more alarming is that the dietary nutrients which are fat soluble are at risk due to the poor absorption of dietary fat. Chronic use of fat blockers may lead to deficiencies of fat soluble vitamins like Vitamins A, D, E and K. These could lead to a host of other health problems (see notes below )eg muscle weakness, poor metabolism of calcium lacking in vitamin D see notes below, oxidative stress, poor blood clotting, declining vision etc


These suppressants give you a false sense of fullness. These usually work by blocking the pathways of the neurotransmitters to the brain e.g. serotonin. The others may work on the leptin and ghrelin hormones. Usually within the first weeks of consumption, appetite suppression could be the greatest after which the effects start to diminish as your body gets used to it. Users have noted weight loss of up to 10% of their body weight. Side effects include insomnia (hmm  not getting proper rest now eh?) addiction and irregular heartbeat. If you are not eating enough, what are you doing about all the other nutrients that your body needs besides those for energy?  For example, the proteins and essential amino acids, all the vitamins, trace minerals etc .. are you throwing the baby out with the bath water?  It’s only a matter of time before serious health concerns surface. Also, when you stop taking these suppressants, how will you handle the call of hunger?


There are some programs which ask you to replace your regular meals with 3 shakes a day and 2 snacks for 12 weeks. The target of which is to limit the daily calorie intake to 800Kcal. Seems like a good idea? You have an approximately 2000 Kcal deficit a day ie lose a little more than about 1 Kg a week , about 20Kg in 12 weeks..  wow!!  Throughout the progression of the program, regular meals are reintroduced until reaching a maintenance phase. It is important that these shakes contain the appropriate levels of vital nutrients eg trace minerals, amino acids and fibre. When nutrients like calcium, iron and fibre are lacking, you may suffer constipation, osteopenia and anemia. But whats more important is that the weight lost from a meal replacement program will usually come not only from the excess fats but also lean muscles ie conversion of stored fats and proteins to energy to continue to power your heart, liver, lungs etc . What this mean is that you will lose muscle tissue and this in turn will lead to a slowdown in your overall metabolism which will mean that you will require less energy at rest to stay alive hence when you reintroduce normal food, you will have excess which will in turn get stored as fat and the weight gain cycle continues except this time, your metabolism is at a slower rate…hmmm  not good!


Elevate your metabolism by increasing your heart rate and incidental activity. These are usually caffeine based. Do you know how much stimulant eg caffeine, is in each of these? In your desire to get quick results, you would be tempted to take even more .. imagine, taking the equivalent in excess of 600mg of coffee each time? You can guess what normally happens when you do so – increase blood pressure and its impact on your cardio vascular health, restlessness, anxiety, insomnia (hmm no porper rest here too!!)  In addition, studies are saying that caffeine increases your cortisol hormone  levels (also released in stress related situations)  and this hormone also breaks down your lean muscle tissue for use as additional energy ( your body is signalling that extra energy is being required, so they start to draw down on both the fat and protein into the mitochondria for production of the extra energy required. So, like the case above, it can eventually make you fatter if your lifestyle doesn’t change. Also, a body at stressed over an extended period can only be expected to deteriorate in time.

So, GURANTEED WEIGHT LOSS? – yes sure, but at what cost to your body? There’s more to weight loss than just seeing the results as you stand on the bathroom scales and looking at yourself in the mirror. You want to look good, feel good and actually BE HEALTHY so that you can have the quality of life you are seeking through weight loss.

So, avoid the gimmicky fancy products like herbal teas, pills and shakes. Give yourself a chance of losing weight forever, through exercise, good sensible nutrition and rest. The best (health wise and sustainability) way to lose weight and keep it off is healthy eating, exercise and rest. See a dietary counsellor, get a personal trainer, talk to your doctor –health coach?; get your metabolic and nutritional health checked through the Metametrix Comprehensive Metabolic Profile (CMP) test. Not fancy but it works.


Vitamin D

What can high-vitamin D foods do for you?

  • Help optimize calcium metabolism
  • Help optimize phosphorus metabolism
  • Help prevent type 2 diabetes, insulin resistance, high blood pressure, heart attack, congestive heart failure, and stroke
  • Help prevent falls and muscle weakness
  • Help prevent osteoporosis while maintaining bone integrity
  • Help regulate insulin activity and blood sugar balance
  • Help regulate immune system responses
  • Help regulate muscle composition and muscle function
  • Help regulate blood pressure
  • Lower risk of excessive inflammation
  • Lower risk of some bacterial infections
  • Support cognitive function, especially in older persons
  • Support mood stability, especially in older persons
  • Help prevent chronic fatigue

Vitamin K

Vitamin K has been finding its way back into the nutrition spotlight, and for good reason. In the past, we’ve traditionally focused on this fat-soluble vitamin as a blood-clotting agent. When we are injured, we cannot stop the bleeding unless our blood can coagulate and form a clot to help seal off the wound. The proteins we need to accomplish this task cannot be recruited into action without vitamin K. (The very name of this vitamin originally came from the German word koagulation.)

Vitamin A

  • What it does in the body
  • Vitamin A is essential, either directly or indirectly, for the function of all the organs in your body and is particularly important for growth and development. Despite the fact that vitamin A was the first vitamin to be discovered, its actions in the cells of our bodies are not well understood at a chemical level.
  • Maintenance of normal vision
  • Our eyes need vitamin A to function effectively as vitamin A is involved in the production of a chemical called visual purple, which helps us to see in dim light.
  • Growth, repair and cell differentiation
  • Vitamin A is necessary for the growth and repair of many body cells including those of bones, teeth, collagen and cartilage. It is also essential for a process known as cell differentiation in which unspecialized cells are modified so that they can perform specific functions. Thus vitamin A plays a central role in tissue development and maintenance.
  • Health of epithelial cells
  • Vitamin A is vital for the formation of healthy epithelial cells. These cells cover the internal and external surfaces of the body and are found in the skin, lungs, developing teeth, inner ear, cornea of the eye, sex organs, glands and their ducts, gums, nose, cervix and other areas. Many epithelial cells produce mucus which is necessary to lubricate body surfaces and protect against invading micro-organisms. For example, the good health of the digestive tract lining is important in protecting against ulcers, and maintenance of the lining of the vagina and uterus is important in fertility.
  • Pregnancy and fetal development
  • Because of its vital role in cell development and differentiation, adequate vitamin A helps to ensure that the changes which occur in the cells and tissues during fetal development take place normally. It may be involved in cell to cell communication.
  • Protection against infection
  • Known as ‘the anti-infective vitamin’, vitamin A plays an essential role in protecting your body from infection. It keeps body surfaces healthy so they can act as barriers to invading micro-organisms. Vitamin A stimulates and enhances many immune functions including antibody response and the activity of various white blood cells such as T helper cells and phagocytes. This immune-enhancing function promotes healing of infected tissues and increases resistance to infection.
  • Other actions
  • Laboratory experiments have shown vitamin A to have antiviral activity. Vitamin A also has antioxidant activity and has a role in protecting against free radical damage which contributes to many common diseases. (See page 417 for more information.) Vitamin A is involved in iron metabolism and storage.
  • Absorption and metabolism
  • The presence of fat and bile in the intestines is necessary for vitamin A absorption. Around 80 to 90 per cent of vitamin A in the diet is absorbed, although this is reduced in older people and those who have trouble absorbing fat, such as pancreatitis, celiac disease and cystic fibrosis sufferers, who may run the risk of vitamin A deficiency. Vitamin A is joined to fatty acids in the intestinal lining, combined with other substances and transported to the liver, which stores 90 per cent of the body’s vitamin A.

Vitamin E

  • Vitamin E is the principal fat-soluble, chain breaking antioxidant in tissues and plasma
  • It is carried directly in LDL cholesterol particle and is the predominant antioxidant in the LDL particle.