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Leptins and Inflammation

by Leon Chaitow, ND DO(more info)

listed in bodywork, originally published in issue 141 - November 2007

You might well think that the topic covered in this article does not have an immediate relevance to bodywork, however, once you have read it I am confident that you will agree that it does.

The theme covered relates to imbalances deriving from hormones produced by white adipose (fatty) tissue (WAT) particularly leptin.

This subject impacts practitioners and therapists of all disciplines who offer health care to people suffering from conditions as diverse as chronic inflammation, autoimmune diseases, neuropathic pain, obesity, diabetes, thyroid hormone resistance (e.g. unexplained hypothyroidism), many cardiovascular diseases, syndrome-X, food cravings, etc.

Bodyworkers (Massage therapists, Osteopaths, Chiropractors, Physiotherapists, etc.) of course do not treat diabetes, or heart disease, or most of the diseases/conditions mentioned above, however, they do treat people who may well be affected by such diseases, as well as presenting with pain, inflammation and/or neuropathic symptoms.

I am grateful to Judith DeLany LMT, with whom I have co-authored three books – for drawing my attention to the fast evolving area of leptin research, and for compiling a summary of this for use in one of our revisions.

Recent research points towards basic lifestyle changes that can have profound influences on the evolution of such diseases – based on evidence relating to leptin and other hormones produced by fatty tissues.

Due to space constraints I will outline only some of the most pertinent information from this review material, with appropriate references that can be used to expand on the summary below:

•    WAT produces hormones that are active participant in regulating physiological and pathological processes, including immunity and inflammation. (Juge-Aubry et al, 2005);
•    Fantuzzi (2005) notes that WAT produces both pro- and anti-inflammatory factors: ‘The current view of adipose tissue is that of an active secretory organ, sending out and responding to signals that modulate appetite, energy expenditure, insulin sensitivity, endocrine and reproductive systems, bone metabolism, inflammation and immunity’;
•    One of the main features of visceral adipose tissue is an inflated waistline, apple-shaped figure (android body type), and increased systemic inflammation. Weight gain in the abdominal region is also a primary indicator of accumulation of WAT, associated with higher risk of developing cardiovascular disease. (Berg & Scherer, 2005);
•    Some of the hormones produced by WAT, including leptin, play crucial roles in the development of type II diabetes, obesity and atherosclerosis, as well as hormonal imbalance (leptin resistance, adrenaline resistance, insulin resistance), with many negative health consequences. (Reilly & Rader, 2003);
•    When working normally, leptin levels rise when adequate food has been consumed, signalling the brain to stop eating and increasing metabolism. When leptin levels drop, because food is not being consumed, appetite is stimulated. If food is still not consumed (skipped meals for example) and leptin levels continue to drop, this signals metabolism to slow down to conserve body fat. Wilding (2001) has stated that one purpose of leptin is to coordinate metabolic, endocrine and behavioural responses to starvation;
•    Budak et al (2006) suggest that leptin and ghrelin [another hormone produced by fat, and an appetite
stimulator] strongly influence reproduction;
•    The range of diseases and processes influenced by leptin and other hormones produced by WAT runs from inflammatory diseases in general, through cardiovascular disease (atherogenic effects), obesity, neuropathic pain, cancer, autoimmune diseases, cravings and much more – as there are leptin receptor sites on the liver, kidneys, ovaries, adipose tissue and gastrointestinal tract;
•    A study of over 1,000 people (Spiegel et al, 2004) has led to the conclusion that people getting less than optimal number of hours of sleep (i.e. eight) show a rise in ghrelin levels, and a drop in leptin levels, leading to increased risk of the symptoms listed above.

Ways to Regain Normal Leptin Levels

A simple plan has been devised (Richards & Richards, 2005) to help regain normal leptin levels and, thereby, balance the hormonal cascade discussed above. Although this plan may not be ideal for everyone, it is presented here for the majority who, it is suggested, should benefit from its use.
The foundation of the plan contains five basic ‘rules’. It is suggested that breaking any of the ‘rules’ or guidelines (below) can lead to setbacks.
Rule 1: Never eat after dinner, not even a snack or glass of wine or juice. Allow 11-12 hours between dinner and breakfast. Generally finish eating dinner at least three hours before bed. This rule allows leptin, melatonin, cortisol, and other chemicals to balance during the night. Night-eating syndrome individuals have abnormal hormonal patterns apparently associated with nocturnal eating. (Geliebter 2001);
Rule 2: Eat three meals a day. Allow five to six hours between meals. This allows insulin levels to drop, glucagon (produced by the liver) to rise, and fat metabolism to start. If this occurs a couple of hours before more food is eaten, fat stores can be utilized until the next food is eaten. Snacking between meals sends the insulin back up and fat stores remain untapped;
Rule 3: Do not eat large meals. Eat slowly and, if overweight, always try to finish a meal when slightly less than full. Eating slowly allows time for hormonal signals to reach the brain before overeating occurs;
Rule 4: Eat a breakfast containing protein. This helps set the hormonal cycles for the day and for the night. Compromising this can have hormonal effects during the day and into the night, disturbing sleep. Weigle et al (2005) have shown that an increase in dietary protein from 15% to 30% of energy, produced a significant weight loss, presumably ‘mediated by increased central nervous system leptin sensitivity’;
Rule 5: Reduce the overall amount of carbohydrates eaten. Garg et al (1992) note, ‘Compared with the low-carbohydrate diet, the high-carbohydrate diet caused a 27.5% increase in plasma triglycerides and a similar increase in [very low density lipoprotein]-cholesterol levels; it also reduced levels of HDL cholesterol by 11%’.

This brief summary suggests that eating regular balanced (low sugar, for example) meals, including a protein breakfast, avoiding snacking between meals and reducing overall carbohydrate intake, and getting enough sleep, can beneficially impact on a huge range of diseases – including those that involve excessive inflammation.

So if you or your patients are overweight, with inflammatory conditions, and/or with any of the long list of diseases, and conditions mentioned by researchers into leptin – the simple changes (‘rules’) advocated could offer a way of beneficially influencing health.

And when it does this represents an example of integrated health care.

References

Berg A and Scherer P. Adipose Tissue, Inflammation, and Cardiovascular Disease. Circulation Research. 96: 939. 2005.
Budak E, Sánchez MF, Bellver J et al. Interactions of the Hormones Leptin, Ghrelin, Adiponectin, Resistin, and PYY3-36 with the Reproductive System. Fertility and Sterility. 85(6): 1563-1581. 2006.
Fantuzzi G. Adipose Tissue, Adipokines and Inflammation. Journal of Allergy and Clinical Immunology. 15(5): 911-919. 2005.
Garg A, Grundy S and Unger R. Comparison of Effects of High and Low Carbohydrate Diets on Plasma Lipoproteins and Insulin Sensitivity in Patients with Mild NIDDM. Diabetes. 41(10): 1278-1285. 1992.
Geliebter A. Night-Eating Syndrome in Obesity. Nutrition. 17(6): 483-484. 2001.
Juge-Aubry C, Henrichot E and Meier C. Adipose Tissue: A Regulator of Inflammation. Best Practice & Research Clinical Endocrinology & Metabolism. 19(4): 547-566. 2005
Reilly M and Rader D. The Metabolic Syndrome: More Than the Sum of its Parts? Circulation. 108(13):
1546-1551. 2003.
Richards B and Richards M. Mastering Leptin. The Leptin Diet: Solving Obesity and Preventing Disease. 2005.
Spiegel K et al. Sleep Curtailment in Healthy Young Men Is Associated with Decreased Leptin Levels, Elevated Ghrelin Levels, and Increased Hunger and Appetite. Annals of Internal Medicine. 141(11): 846-850. 2004.
Weigle D et al. A High-Protein Diet Induces Sustained Reductions in Appetite, Ad Libitum Caloric Intake, and Body Weight Despite Compensatory Changes in Diurnal Plasma Leptin and Ghrelin Concentrations. Am J Clin Nutrition. 82(1): 41-48. 2005.
Wilding J. Leptin and the Control of Obesity. Current Opinions in Pharmacology. 1(6): 656-661. 2001.

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About Leon Chaitow, ND DO

Leon Chaitow ND DO - December 7, 1937 — September 20, 2018 was a registered Osteopath and Naturopath and an Honorary Fellow at the University of Westminster. He has been author of over 70 books, edited the peer reviewed Journal of Bodywork & Movement Therapies, and practised in a NHS Health Centre and privately. He taught widely to Physiotherapists, Osteopaths, Chiropractors and Massage Therapists. Further information about Leon who sadly died 20 September 2018 is available via his website: www.leonchaitow.com

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