Excessive amount of visceral fat is considered a crucial indicator for metabolic syndrome, and is also associated with cardiovascular disease, liver injury and increase risk of Type 2 diabetes. Early detection is essential for prevention of these diseases. Waist circumference (WC), fat mass, body mass index (BMI), body volume index, visceral fat area and waist-hip-ratio, all can predict visceral adiposity in abdominal obesity. The absolute waist circumference (>102cm in men and >88cm in women), and the waist-hip ratio (circumference of the waist divided by that of the hips of >0.9 for men and >0.85 for women), are both used as measurement of obesity. For given WC, the type of obesity can be determined bioelectrical impedance and body volume index measurement. Visceral fat area (VFA) at the umbilicus level measured by CT is adopted as the gold standard, but it has many limitations. Recently, application of abdominal bioelectrical impedance analysis (BIA) for measuring VFA is widely used.
The measurement of ALT liver enzyme is associated with truncal/visceral fat accumulation, metabolic syndrome, raised BMI, hyperleptinemia, and hyperinsulinemia. This metabolically active fat induces non-alcoholic fatty liver disease with raised ALT levels. Obesity raises serum resistin levels, which in turn directly correlate to insulin resistance. Studies have also confirmed a direct correlation between resistin levels and Type 2 diabetes; and it is central obesity which seems to contribute to increasing levels of serum resistin. Serum resistin levels have been found to decrease with weight loss. Enzyme-linked immunosorbent assay (ELISA) tests detect circulating resistin protein levels. This is, therefore, a useful test to confirm metabolic syndrome.
Low Calorie Diets
It has long been known that low calorie diets increase longevity and help prevent leading causes of death such as inflammatory diseases like cardiovascular disease and cancer. The mechanisms through which life extension occurs include improved mitochondrial functioning, activation of sirtuin genes (longevity genes), obesity reduction, and anti-inflammatory effects.
To keep in mind, though, being on a low calorie diet is not to become nutritionally compromised, or nutrient depleted or osteopenic or osteoporotic. Often, dietary supplementation may become necessary with low calorie diets. Of great help would be to make use of calorie restriction mimetics. These mimetics give one the same effects of decreased calorie intake without the need to starve oneself and don’t have the weight loss effects associated with low calorie intake, but do have the life extending effects comparable to those seen with low calorie intake. These mimetics switch off cancer genes, switch on longevity genes, and reduce inflammation and improve mitochondrial functioning, too.
While all diets don’t offer the secret to living life thinner, calorie restriction certainly has far-reaching benefits for longevity. This is where calorie restriction mimetics (CRM) come into play. There are a number of naturally occurring factors (from peptides and alkaloids to polyphenols and amino acids) that mimic the anti-aging effects of calorie restriction and show the same physiological effects. CRM can be described as a chemical compound or natural agent that can be reproduced (or mimic) one or more principle biological effects of calorie restriction. There is a great deal of versatility in using CRM, as some may affect genetic controls of aging and others may be more specific to glucose metabolism, for example.
CRM isn’t a magic bullet in terms of weight loss. However, the longevity effects are far too considerable to be taken lightly. Speak to you healthcare practitioner about taking CRM supplements to induce long life, wellness and overall well-being.
• Resveratrol (100mg twice daily)
• Pterostilbene (50mg twice daily)
• Carnosine (500mg twice daily)
• Grape seed extract (100mg twice daily)
• Alpha lipoic acid (R-forms) (150mg twice daily)
• Acetyl-L-carnitine (500mg to 1,000mg twice daily)
• Metformin (on prescription only) with vitamin B12 if insulin resistant
• Good quality complete antioxidant formula
Success in Weight Loss Requires a Multi-faceted Approach
Cortisol Excess and Adrenal Fatigue
Elevated cortisol caused by stress or aging puts the body into a fat-storage mode. Adrenal stress causes craving for coffee, soft drinks and sugar.
• DHEA (dehydroepiandrosterone) is an adrenal hormone that decreases in tandem with the aging process. DHEA opposes the fat-storage effects and cravings caused by elevated cortisol.
• Rx Women: 0.5 to one tablet (12.5mg to 25mg) daily.
• Rx Men: one to two tablets (25mg to 50mg) daily, as a single day dose (after breakfast)
Herbal adaptogens contain adrenally-supportive herbal extracts (Rhodiola rosea and Ashwagandha). These stimulate the adrenals during low adrenal function (adrenal fatigue), and calms adrenal function (and excessive cortisol release) during adrenal stress.
Insulin Resistance, Metabolic Syndrome and PCOS
Insulin resistance is a common cause of weight gain and PCOS, and makes weight loss difficult.
• D-Chiro-Inotisol is an insulin-sensitizing nutrient that improves the body’s responsiveness to insulin.
• Rx: one capsule daily or twice daily, after meals
Other nutrients to aid with insulin resistance include:
• Irvingia Plus Fat Burner: one capsule twice daily, 20 minutes before meals
• HCA and chromium: one to two caplets, 20 minutes before each meal (with chromium for decreasing insulin resistance)
• Alpha Lipoic Acid: one capsule twice daily
• 7-Keto DHEA: 25mg per day
• Krill Oil OR Fish Oil Extract Omega 3: two capsules daily
• Vitamin D3: typically doses of 2000iu per day depending on vitamin D levels
Leptin resistance has a lot in common with insulin resistance.
Adipocytes (fat cells) are the primary cells for fat storage. Leptin is released by adipocytes to perform two critical functions. First, it signals the brain that enough food has been ingested and shuts down appetite. It then seems to initiate a process whereby the stored triglycerides (the form that most fat exists in the body) in the adipocytes are broken down into fatty acids that can be used for energy production.
The size and number of adipocytes increase with weight gain. They then release more and more leptin into circulation in an attempt to tell the brain that fat stores are adequate, and appetite needs to be controlled. However, because these same fat cells are now constantly surrounded by elevated levels of leptin, they progressively lose sensitivity for this leptin that they are producing in excess. Inadequate sensitivity results in reduced responsiveness. With two outcomes: first, normal fatty acid oxidation (fat burning) within adipocyte becomes less likely to absorb free fatty acids from circulation. This resulting excess of fatty acids floating in the bloodstream causes a functional insulin resistance in tissues.
Eating habits can cause havoc in the body’s communication system that dictates metabolism and appetite. Consistent overeating confuses the efficient transmission of messages, causing a breakdown that leads to weight gain, and additional consequences such as heart disease. Fat used to be viewed only as a storage place in the body for extra calories. However, we now know that it’s actually an endocrine organ. The fat that we moan and groan about when it accumulates on our thighs, buttocks and abdomen could ironically keep us lean. This white adipose tissue secretes the hormone leptin, which informs the brain about our levels of fat, telling us when to eat and when to stop eating.
Leptin is normally secreted in a circadian rhythm, with as many as 32 pulses of activity occurring over a 24-hour period. The highest levels are found during the first few hours of sleep, decreasing to the lowest in the morning. In obese people, the change in blood leptin levels is less significant than in lean people. One of the reasons for this is that an excess consumption of food has a negative impact on leptin’s ability to communicate adequately with the brain. This results in insulin, thyroid, epinephrine and leptin resistance, and potential weight gain.
If there’s leptin resistance, the brain doesn’t register signals to reduce appetite, leaving a person feeling constantly hungry. Normally, when you’ve eaten sufficiently, the brain receives a signal that leptin levels are high, and it increases metabolism and decreases appetite. Conversely, when your body needs food, the brain tells you to eat. When this process is inhibited by bad eating habits, your brain doesn’t know to tell you when to stop and excess calories are sent to storage as fat. Increased levels of triglyceride (a type of fat found in your blood) caused by overeating, have been linked to leptin resistance. This fat decreases the transport of leptin across the blood brain barrier, preventing leptin from entering the brain.
Leptin inhibits insulin secretion in the pancreas, and when your body is resistant to leptin, the pancreas isn’t able to sense it and keeps making insulin, leading to an excess and the possibility of insulin resistance – another cause of weight gain.
Yet another cause of leptin-resistant weight gain is tied in with epinephrine, a hormone and a neurotransmitter that is a prime factor in the body’s fight or flight response, increasing heart rate, constricting blood vessels and dilating air passages when the body senses danger. Epinephrine has short-term control of leptin and when the body’s sympathetic nervous system is activated in quick bursts during moments of panic, leptin production is depressed. The brain uses epinephrine to stimulate metabolism in fat cells and if the brain is repeatedly attempting to use this hormone to no effect, unusually high levels can occur, and fat cells eventually become immune to it. This resistance leads to weight gain, specifically in abdominal area, which is most often associated with reproductive organ cancer and heart disease.
A resistance to leptin produces “false starvation”, slowing thyroid function even in overweight people. Leptin and thyroid resistance restrict the natural heat production in the body, as fat and calories aren’t efficiently burned away.
To ensure the body’s optimal functionality, it’s important to listen to the brain’s messages. However, if our bad habits inhibit the brain’s ability communicate effectively, we can get stuck in a rut of silent rebellion. A lifestyle change, specifically in terms of eating habits, as well as supplementation, will greatly assist in getting your body back in line. While in a diet high in carbohydrates and saturated fats is a definite no-no if you are leptin resistant, a “high good fat” diet has shown successful results. Stock your pantry (and plate) with monosaturated fats like olive oil, canola oil, avocados, nuts and seeds, olives and dark chocolate, and listen up for leptin’s long-forgotten call.
Protocol for Decreasing Leptin Resistance
Irvingia Gabonesis is a herb showing remarkable success as a viable form of leptin resistance treatment. This herb also lowers cholesterol levels as well as fasting glucose levels. It also reduces the C-reactive protein that binds leptin and makes one resistant to it. Using this herb alone can help correct leptin resistance. Resveratrol and green tea extracts such as EGCG are useful.
Neurotransmitters and Weight Loss
Low levels of brain serotonin are commonly associated with food cravings.
• 5-hydroxy-trytrophan (an amino acid) is the direct precursor of serotonin. Unlike SSRIs, which are serotonin re-uptake inhibitors, and can cause weight gain, serotonin precursors, such as 5-HTP, reduce appetite and cause weight loss.
• Rx: one to two capsules (100mg to 200mg) twice daily, on an empty stomach
Fiber Intake and Weight Loss
An adequate intake of fiber is important for weight loss because it lowers the glycemic index (GI) of meals and promotes a feeling of fullness.
Inflammation, Liver Detoxification and Weight Loss
Fat is metabolized under the control of a hormone called leptin. Sub-clinical inflammation causes the release of leptin-desensitizing inflammatory molecules such as C-reactive protein (CRP). When leptin sensitivity is reduced, weight loss becomes more difficult. Furthermore, any weight loss program places an increase burden on the liver, due to metabolized fat for releasing accumulated stored toxins into the blood stream. Supporting Phase 2 liver metabolism, to flush out circulating toxins, is an important part of any weight loss program.
• Curcumin: Curcumin is extracted from turmeric spice. It reduces CRP and other inflammatory markers. Curcumin also supports Phase 2 liver detoxification with piperine for enhanced absorption.
• Silibinin: milk thistle extract is extremely useful in detoxifying the liver and helping with blood glucose and cholesterol management.
Sleep, Melatonin and Weight Loss
Studies show that lack of sleep is associated with weight gain, insulin resistance and elevated cortisol. Elevation of yet another hormone called ghrelin also leads to weight gain with sleep deprivation.
Melatonin and Melatonin Slow Release
• Melatonin is responsible for healthy sleep architecture. It exhibits no addictive or tolerance-inducing properties. It is available in standard formulation for patients exhibiting difficulty falling asleep, and in slow release form, for patients who can’t maintain sleep.
• Rx: one tablet (3mg) at bedtime
Additional Weight Loss Nutraceuticals
CLA (Conjugated Linoleic Acid)
CLA is a naturally occurring fatty acid. Clinical trials have shown that usage promotes weight loss (2000mg twice daily after food).
Studies show that L-carnitine (an amino acid) aids in weight loss by converting stored fat into energy. Taking 1400mg of L-carnitine twice daily, with or without food, may assist with weight loss.
Hursting SD,Lavigne JA, et al. Calorie restriction, aging and cancer prevention: mechanism of action and applicability to humans. Ann Rev Med. 2003;54131-152
Holt S Specific anti-aging factors for natural clinicians. Townsend Letter Jul 2008:90-6
Tsai AG, Wadden TA. Systematic review: an evaluation of major commercial weight loss programs in the United States. Ann Intern Med 2005;142:56
Melanson E, Astrup A, Donahoo W. The Relationship between Dietary Fat and Fatty Acid Intake and Body Weight, Diabetes, and the Metabolic Syndrome. Ann Nutr Metab 2009;55:229-243
Stern L, Iqbal N, Seshadri P, et al: The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med 2004;140:778
Skov AR, Touro S, Bulow J, et al: Changes in renal function during weight induced by high vs low-protein low-fat diets in overweight subjects. Int J Obes relat Metab Disord 1999;23:1170
Votruba SB, Horvitz MA, Schoeller DA: The role of exercise in the treatment of obesity. Nutrition. 2000;16:179
Trayburn P, Beattie J. Physiological role of adipose tissue: white adipose tissue as an endocrine and secretory organ. Proc Nutr Soc. 2001;60:329-39
Radi R, Nikoli V, et al> Circadian rhythm of blood leptin level in obese and non-obese people. Call Antropol. 2003;27:555-61
Kalra S. Central leptin insufficiency syndrome: An interactive etiology for obesity for obesity, metabolic and neural diseases and for designing new therapeutic interventations. Peptides. Jan 2008;29(1):127-38
Banks W, Coon A, et al. Triglycerides induce leptin resistance at the blood-brain barrier. Diabetes. 2004;53:1253-60
Seufert J. Leptin effects on pancreatic beta-cell gene expression and function. Diabetes. 2004;53(1):152-8
Zhang C, Rexrode K, et al. Abdominal Obesity and the Risk of All-Cause, Cardiovascular, and Cancer Mortality. Sixteen Years of Follow-Up in US Women. Circulation. 2008;117:1658-67
Huo L, Munzberg H, et al. Role of signal transducer and activator of transcription 3 in regulation of hypothalamic trh gene expression by leptin. Endrocrinology. 2004;145:2516-23
Wiegle D, Cummings D, et al. Roles of Leptin and Ghrelin in the Loss of Body Weight Caused by Low Fat, high Carbohydrate Diet. The Journal Clinical Endocrinology & Metabolism. Apr 2003;88(4):1577-86