Archive for the ‘Dieting’ Category

Watching what you eat: foods having delayed effect on appetite

November 28, 2011

On a very low energy diet(often called VLCD), the dieter starts considering each additional item of  food or drink on the basis of the energy it will add.   Science has provided another basis for considering foods:  the subsequent effect on appetite.  I want to list a few where it will be interesting to watch for future research:

1. Milk products:  In those with a low calcium intake, reduce feelings of hunger more than an energy-matched drink. The calcium and protein in milk may be the triggers for this effect.(1, 2)

2. fats and oils

The short-term effect of fats is to reduce the sensation of hunger shortly after the fatty acids from digestion of fats reach the duodenum.   Surprisingly small amounts of oil can have this effect, but in those who eat much fat it is suppressed –  the whole matter of fat digestion is horribly complex (3)   However, improved sensitivity was measured in obese men after 4 days on a VLCD . (4)

Unfortunately, it has been found that eating fats/oils  does not always reduce appetite later, and may increase appetite the next day (5).   This fits with anecdotal evidence – for example, following a cheesecake relapse, a dieter experienced more hunger than usual the next two days, where the same effect was not felt after a protein-binge.

More confusingly, the type of oil is important – for example, fish oil seems to add less energy (that is, result in less fat) than do maize oil or beef fat. (6)

3. Citrates

Lemon juice, and various similar chemicals often added to cordials.   In some people, citrates seem to make it more difficult to adhere to a VLCD.  This may be linked to  the role of citric acid in favouring gluconeogenesis over ketogenesis (7).  (VLCDs emphasise ketogenesis for weight loss.  Making glucose inside the body does burn energy, but seems linked to increased appetite

Research needed:

Most studies emphasise same-day or long-term effects of particular food types.   More reliable studies on two- or three-day effects on appetite and perceived tiredness/energy levels, with titles showing on net searches, would be welcome.

———————————————————————————-

Footnotes
1. Gilbert JA, Joanisse DR, Chaput JP, Miegueu P, Cianflone K, Alméras N, Tremblay A.   (2011)  “Milk supplementation facilitates appetite control in obese women during weight loss: a randomised, single-blind, placebo-controlled trial.”     Br J Nutr. 105(1):133-43.   http://www.ncbi.nlm.nih.gov/pubmed/21205360

2. Major GC, Alarie FP, Doré J, Tremblay A. (2009) “Calcium plus vitamin D supplementation and fat mass loss in female very low-calcium consumers: potential link with a calcium-specific appetite control.” Br J Nutr. 101(5):659-63. http://www.ncbi.nlm.nih.gov/pubmed/21205360

3. Little, Tanya J. and Feinle-Bisset, C  (2010)  “Oral and Gastrointestinal Sensing of Dietary Fat and Appetite Regulation in Humans: Modification by Diet and Obesity” Front Neurosci. 2010; 4: 178. Published online 2010 October 19. Prepublished online 2010 May 20. doi:  10.3389/fnins.2010.00178   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981385/

4.

Brennan, I M,  Seimon, R V, Luscombe-Marsh, N D, Otto, B, Horowitz, M and Feinle-Bisset C (2011). “Effects of acute dietary restriction on gut motor, hormone and energy intake responses to duodenal fat in obese men” International Journal of Obesity 35, 448–456; doi:10.1038/ijo.2010.153; published online 3 August 2010  http://www.nature.com/ijo/journal/v35/n3/abs/ijo2010153a.html

5.http://www.reebokcrossfitone.com/Nutrition/Effect-of-dietary-fat-on-satiation-within-and-between-meals.html?print=1&tmpl=component (does not display well in my browser, but deserves credit for links to the fulltext article

Blundell, JE, Burley, VJ,  Cotton, JR, and Lawton CL  (1993) “Dietary fat and the control of energy intake: evaluating the effects of fat on meal size and postmeal satiety.”  American Journal of Clinical Nutrition, Vol 57, 772S-778S  http://www.ajcn.org/content/57/5/772S.abstract?sid=d31ef1ca-bb08-4d39-9f0b-ec12322c5e74)

6.Jang IS, Hwang DY, Chae KR, Lee JE, Kim YK, Kang TS, Hwang JH, Lim CH, Huh YB, Cho JS. (2003) “Role of dietary fat type in the development of adiposity from dietary obesity-susceptible Sprague-Dawley rats.”  Br J Nutr. 2003 Mar;89(3):429-38. http://www.ncbi.nlm.nih.gov/pubmed/12628037

7. Kreitzman, S.N. (1992)  Factors influencing body composition during very-low-calorie diets   Am J Clin Nutr 56:217S-23S.

Advertisements

“It’s Just Water” … well, no. Early weight loss in dieting.

November 7, 2011

One of the common statements in low-energy dieting is that “The first couple of kilos is just water.”   (That is, once you allow for the change in bowel contents.) If it is just water, how can one lose two litres of water and not feel the effects of dehydration?

To understand this, we have to understand a little human  biochemistry.

Glucose,  glycogen stores, and water

Our brains and muscles “burn” glucose – a simple sugar, found in many carbohydrate rich foods (for example, cane sugar is one fructose molecule bound to one glucose molecule).   It  is disassembled to release chemical energy, carried in the form of a small molecule called ATP (Adenosine triphosphate).   Glucose is so important that our bodies can use other molecules and energy from other foods to make glucose (gluconeogenesis).

As with other important materials, our bodies store glucose for later use.  The stores are not glucose itself – they are molecules which the body can take apart for glucose.  The first storage is as a molecule called glycogen, stored in the liver and muscles;  secondary storage is as fat.  When there is plenty of glucose and ATP,  insulin promotes the conversion of glucose into glycogen.

When there is little ATP and little glucose, our cells’ first response is to disassemble glycogen to keep the blood sugar level up.   So, in dieting, our cells first use the glycogen stores. A common estimate of adult glycogen stores is 400 to 500 g.   However, glycogen is not stored alone – like glucose, its pure form is not a soft or liquid substance.  It is stored with three to four times its weight in water (1).   So, in the initial stages of dieting, the glycogen stores are used up and the associated water is released.

It takes energy to make and store glycogen, and to transport its related water.  So, in using up glycogen, dieters  reduce the stored energy within their bodies.   Therefore, the weight loss is not just water, and does reflect a real improvement in body mass – just not as much in terms of fat-equivalents.

After the diet

When the dieter returns to a weight-maintenance eating pattern, it is reasonable for ver to rebuild ves glycogen stores.  So, ve must plan for that: ve must be aware that the first couple of kilos (after accounting for bowel contents) will not be fat, will be valuable for maintaining blood sugar levels, and are to be expected to be back very soon after leaving off the strict regimen (in days, not weeks.)  An immediate effect is that the target weight should reflect this expectation: if ve wishes to weigh 65 kilos, ver goal in dieting would be 63 kilos (minus an amount  for bowel contents depending on diet) .

Upsides and downsides of continuing low-energy dieting for more than the water-loss period

Upside

The body does not burn its fat stores significantly until the glycogen is low.   This is one reason to value the rapid initial glycogen and water weight loss stage, and to continue beyond it.

A second reason is not commonly known:  the brain relies on glucose for energy until blood sugar levels have been low for some time, but after about three days it starts using smaller molecules called ketone bodies (the things which give dieters ketosis, resulting in  “nail polish breath (2) “).  From about 40% after three days of starvation (3), after about a month it can get up to 7o% of its energy from ketone bodies.  In human evolution periods of  low-carbohydrate diets  – and real hunger – were common, so is reasonable that our bodies are adapted to use other energy sources.  It is now suggested that there may be benefits to deliberately triggering this shift in brain metabolism. (4)  As with decreased exposure to diseases with modern lifestyles (5,6), decreased exposure to hunger may not be entirely to our benefit.

Downside

There is one main downside:   Low blood sugar is linked to various problems, including difficulty  controlling impulses.  In dieting these are not as severe as those diabetics may experience , but a degree of crankiness is to be expected – especially in the days before the brain shifts to using ketone bodies.

A second downside is the risk that low energy intake may be associated with a poorly balanced diet with poor essential nutrient levels.  One may get away with this in the short term, but over longer periods one must plan very carefully.   I feel that this is minor, as there are several well balanced VLCD (very low calorie diet) systems available.  However, unless the dieter is competent in dietary analysis, it would be best to have nutritional advice from a University-trained source.

A third downside is that the process is a physical strain – which is why the packaged approaches recommend medical supervision: there is a risk that unrecognised problems (such as liver failure) may flare up under the stress.

Conclusion

It isn’t just water, and it is a sign that you are, at least, not getting fatter.  The hard work is worth it – but watch your temper and watch your nutrition.

_____________________________________________

1.  Kreitzman, S N  (1992)  Factors influencing body composition  during very-low-calorie diets Am J Clin Nutr 56:217S-23S.   http://www.ajcn.org/content/56/1/217S.long

2. Note that this mild ketosis is different from the severe and life-threatening ketoacidosis (commonly from diabetes or alcoholism), where the smell is stronger and medical attention is required.

3.Hasselbalch, SG; Knudsen, GM; Jakobsen, J; Hageman, LP; Holm, S; Paulson, OB (1994). “Brain metabolism during short-term starvation in humans.”. Journal of cerebral blood flow and metabolism 14 (1): 125–31. doi:10.1038/jcbfm.1994.17. PMID 8263048.

4. http://www.ncbi.nlm.nih.gov/pubmed/20188215   , http://www.ncbi.nlm.nih.gov/pubmed/20009300

5. Committee on The International Study of Asthma, Allergies in Childhood (ISAAC), Steering Committee. Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema. ISAAC Lancet. 1998. pp. 1225–32.

6. Nowak D, Wichmann H-E, Magnusson H. Asthma and atopy in Western and Eastern communities- current status and open questions. Clin Exp Allergy. 1998;28:1043–6. [PubMed]