Your great grandmother is proven right – the best food to eat, and to control your weight, is the traditional diet (aka the leptin diet)
Thanks to Leon Chaitow for the content of this article (more info at www.leonchaitow.com)
Number one rule is avoid snacking. That’s also the number two and three rule, but not because it reduces the amount you eat, but because of body rhythms. It’s all about balancing leptins, the hormone that makes you notice when you are full and which is produced in your adipose layer (that’s the fat under your skin to you).
Summary of ‘Leptin’ Based Guidelines
- Eat a breakfast containing significant protein content
- Eat 3 meals a day – 5 to 6 hours between each
- Avoid snacks
- Never eat after dinner
- Allow 11-12 hours between dinner and breakfast
- Generally finish eating dinner at least 3 hours before bed
- Do not eat large meals
- Eat slowly
- Reduce the overall amount of carbohydrates eaten, (e.g cereals/fructose !) and consider increasing at intake
- Get adequate exercise
- Ensure 7 hours sleep per night at least
- Enhance stress coping strategies
- Supplement with calcium, omega 3 oil, probiotics, vitamin D, Acetyl-L-Carnitine if indicated
- Control gut overgrowth of candida & other fungi
Obesity, leptin and ghrelin
Leptin and ghrelin are two hormones with a major influence on energy balance.
Leptin mediates long-term regulation of energy balance, suppressing food intake and so inducing weight loss.
Ghrelin is a fast-acting hormone, that plays a role in meal initiation.
With obesity incidence rising, understanding the mechanisms by which these (and other) substances influence energy balance has been a subject of intensive research
In obesity circulating level of the leptin (satiety) hormone is increased, whereas surprisingly, the level of ghrelin (appetite inducing) is decreased.
It is now established that obese patients are leptin-resistant.
How this happens seems to relate to lifestyle (e.g. exercise & sleep patterns), as well as to food choices, and the timing of meals.
(Klok et al 2007 .The role of leptin and ghrelin in the regulation of food intake and body weight in humans: A review(2007) Obesity Reviews, 8(1):21-34).
- Discovered in 1994, leptin hormone was first thought to simply signal satiety (hunger satisfaction)
- Peripheral actions of leptin interface with insulin biosynthesis and, with leptin receptors on the Pancreas (Fehmann et al 1997).
- In return, insulin stimulates leptin secretion from adipose tissue (Havel 2002), establishing a hormonal regulatory feedback loop.
- Leptin is secreted by abdominal, thigh & buttock WAT
- It has a regulatory effect on thyroid, adrenal, pancreatic and sex hormones (Havel 2000) and plays an important part in body weight regulation, eating behavior, and reproduction. (Budak et al 2006)
(Halle M, Persson P 2003 Role of leptin an leptin receptor in inflammation. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology 284(3) R760-R762
Budak E, Sánchez MF, Bellver J et al 2006 ?Interactions of the hormones leptin, ghrelin, adiponectin, resistin, and PYY3-36 with the reproductive system. Fertility and Sterility 85(6):1563-1581
Fehmann H, Berghöfer P, Brandhorst D, et al 1997 Leptin inhibition of insulin secretion from isolated human islets. Acta Diabetologica 34(4):249-252)
Are Cereals to blame for leptin resistance?
Jonsson et al (2005) suggest that humans (and the leptin system) are not well adapted to a cereal-based diet, and that leptin resistance could be a sign of insufficient adaptation away from hunter-gatherer patterns of eating.
They further propose that lectins (a constituent of cereals) have properties that can cause leptin resistance, either through effects on metabolism central to the proper functions of the leptin system, and/or directly through binding to human leptin or the human leptin receptor
These researchers conducted a study on 24 domestic pigs in which a cereal-free hunter-gatherer diet promoted significantly higher insulin sensitivity, lower diastolic blood pressure and lower C-reactive protein, as compared to a cereal-based swine feed
(Jönsson T et al 2005 Agrarian diet and diseases of affluence – Do evolutionary novel dietary lectins cause leptin resistance? BMC Endocrine Disorders 5, art. no. 10)
Leptin resistance….snacks as a culprit??
- Hunter gatherers store energy as fat when food supplies are erratic.
- Today we may not have digested the previous meal before more food is consumed.
- Cutler et al (2003) suggest extra calories from snacks are the weight gain culprit, with a 60% rise in average number of daily snacks since early 70s.
- Howarth et al (2006) report that in both younger and older adults “eating frequency is positively associated with energy intake, and eating more than three times a day is associated with being overweight or obese.”
(Cutler D et al 2003 Why have Americans become more obese? Journal of Economic Perspectives 17(3):93-118
Howarth N et al 2006 Eating patterns and dietary composition in relation to BMI. Int.J Obesityhttp://www.nature.com/ijo/journal/vaop/ncurrent/abs/0803456a.html)
Does low fat, or low carbohydrate, diet produce satiety more effectively, via PYY?
- Peptide YY (PYY) is released from the distal small intestine and colon after meals and reduces appetite by increasing satiety.
- The amount of PYY released is proportional to calories ingested
- A study, involving 18 obese subjects, was conducted to determine whether macronutrient composition influences postprandial serum PYY levels by comparing:
- 1 wk of a weight-maintenance low-carbohydrate, high-fat (LCHF) diet
- 1 week of a low-fat, high-carbohydrate (LFHC) diet.
Results showed that a low-carbohydrate, high-fat LCHF diet stimulates PYY secretion more than a LFHC diet in obese individuals
(Essah P et al 2007 Effect of macronutrient composition on postprandial peptide YY levels Journal of Clinical Endocrinology and Metabolism 92(10):4052-4055)
Exercise and Leptin Sensitivity
- Changes in body composition and metabolism during a lifestyle intervention were investigated in 23 older, obese men and women with impaired glucose tolerance
- All undertook 12 wk of aerobic exercise training, 5 days/wk for 60 min at 75% maximal oxygen consumption, with either normal caloric intake (eucaloric group) or a reduced-calorie diet (hypocaloric group)
- Body composition, aerobic fitness, leptinemia, insulin sensitivity, and intra-myocellular lipid accumulation (IMCL) in skeletal muscle improved in both groups (P < 0.05).
- Improvements in body composition, leptin, and basal fat oxidation were greater in the hypocaloric group
- Exercise training helps create a metabolic milieu that promotes lipid use in skeletal muscle, so facilitating a reversal of insulin resistance
- At the same time leptin sensitivity is improved, but this trend may rely on reducing caloric intake as well as exercise training
(Solomon T et al 2008 Exercise and diet enhance fat oxidation and reduce insulin resistance in older obese adults. Jnl Applied Physiology 104(5):1313-1319)
High Fructose Intake Leads to Leptin Resistance in Rats
A Recent study suggests that the consumption of high amounts of fructose causes leptin resistance, and elevated triglycerides, in rats.
The high fructose diet rats subsequently ate more and gained more weight than controls, when fed a high fat, high calorie diet.
Shapiro A et al 2008 Fructose-induced leptin resistance exacerbates weight gain in (response to subsequent high-fat feeding. Am.J Physiology. Regulatory, Integrative and Comparative Physiology, 295(5):1370-1375)