Key Factors For Successful Weight Loss

Key Factors For Successful Weight Loss

Key Factors For Successful Weight Loss

Worldwide the rate of obesity has almost doubled over the past 30 years. For many achieving a healthy body weight represents an ongoing struggle despite their genuine efforts to reduce food consumption and increase energy expenditure. Recent scientific research has provided a new perspective on the biology of weight loss which is much more than the popular and simplistic idea of “eat less to lose weight”. For any weight loss plan to be successful, it must provide beyond the conventional cliché that weight loss only requires a reduction in food consumption. Successful weight management requires to acknowledge and address the multi-factorial nature of obesity.

Body Weigh Regulating Process:

The human body has evolved to ensure maintaining adequate energy reserves to sustain life during food scarcity and famine. Abundance and access to the variety of food are relatively recent.

Body weight maintenance involves very complex and interrelated interactions between neurological and hormonal factors, to regulate appetite and preserve body energy stores. Hypothalamus in the brain monitors and integrates neurological signals and modulates appetite accordingly.

Sensory cells of the stomach detect stretching of stomach tissue and via nerve impulses directly signal satiety to the brain. Blood levels of glucose, fatty acids, and amino acids stimulate the perception of satiety in the brain.

Also, a variety of hormones with various levels are released in the gastrointestinal tract to balance energy intake and utilization of nutrients. For example; Insulin from the pancreas is critical for glucose uptake by cells of the body; and cholecystokinin (CCK) from the upper part of the small intestine is important to trigger release of digestive enzymes and bile. Both Insulin and CCK provide potent satiety signals.

Fat cells relay their storage status to the brain by secreting Leptin hormone. Leptin acts on the hypothalamus, stimulating the release of neurotransmitters that signal satiety, and suppressing those that signal hunger. Therefore, leptin provides the brain with information on long-term energy status and allows it to adjust food intake.

However, in obesity, excess fat stores contribute to chronically elevated leptin levels and the brain cells gradually lose their sensitivity to leptin, causing a physiologic state known as leptin resistance in which the brain no longer responses to it; thus, it neither produces satiety neurotransmitters nor stops the hunger . Most of the weight loss efforts are not successful due to failure of the leptin system to suppress appetite, resulting in excessive hunger.

Fat cells are also releasing a hormone called adiponectin, which is an anti-obesity signaling hormone. Adiponectin signaling is also disrupted in obesity-related diseases and states of insulin resistance. Evidence suggests that leptin and adiponectin can work together to combat insulin resistance.

This further suggests that optimizing fat cell signaling to be considered as an important aspect of any comprehensive weight-loss strategy.

Resting energy expenditure (REE) represents the rate of calorie burnt due to metabolic activities during resting periods. Therefore, low REE may contribute to weight gain or make it difficult to lose weight. Studies show that REE is directly related to serum adiponectin levels, and that higher leptin levels. Aging is also associated with low REE. These findings suggest that boosting REE could be valuable to manage age-related weight gain.


Interrupting Factors to Body's Weight Regulating Process?

The natural aging is associated with hormonal changes, in particular, decreases in sex and thyroid hormones, contributing to lower metabolism and resting energy expenditure. It is also linked to reduced insulin sensitivity which can interfere with appetite control. Lack of physical activity and loss of muscle mass, means lower usage of calorie from food .

Obesity and low testosterone have a complex relationship; low testosterone is considered both a cause and effect of weight gain. an increased fat mass in men may contribute to the conversion of testosterone to estrogen by the aromatase enzyme. While this is a normal process, aromatization is happening more in fat tissue.

In women, estrogen levels decline suddenly with menopause; and based on years of documents, hormone replacement does not provide a consistent benefit to reduce abdominal fat in women.

The thyroid gland is the master metabolism regulator; thyroid hormone (thyroxine or T4) influence metabolism in different tissues of the body. Thyroid disorders affect body weight, temperature, and energy independent of physical activity. Low thyroid function (hypothyroidism) causes reduced conversion of stored energy into heat and metabolic rate promoting weight gain. A significant number of obese patients show elevated thyroid stimulating hormone (TSH) levels which is indicative of low thyroid function.

In addition to be resulted from obesity, elevated levels of the leptin and insulin in obese individuals can be indicative of a resistance to their activities. Insulin helps facilitate cellular uptake of glucose, mainly in the muscles, liver, and fat tissue. In insulin resistance, glucose levels are not efficiently controlled by the action of insulin causing high blood sugar level. In addition, while higher levels of both leptin and insulin should suppress the desire to eat and stimulate energy expenditure, it seems they are unable to provide this function in resistant individuals.

Increased inflammatory biomarkers such as C-reactive protein (CRP) is common in both Insulin and leptin resistance conditions. Results from animal studies suggest that high CRP level counteracts with the leptin function. Therefore it has to be considered as a part of the weight management program.

While serotonin levels are mainly known to play a role in mood regulation, It has also been linked to weight. Serotonin interacts with the brain receptors which regulate appetite. Higher level of serotonin causes less desire to eat, but as serotonin levels drop, appetite is stimulated. Studies have shown that obese individuals have low levels of tryptophan amino acid which is a precursor to serotonin, suggesting that restoring serotonin signaling may be beneficial to manage cravings.

Exposure to chronic stress has been a contributing to obesity and metabolic syndrome in human and animal studies. Stress increases the cortisol production which contributes to weight gain in different ways. Fat cells contain more receptors for cortisol, Interaction between cortisol and its receptors of the fat cells, produces a signal of storing more fat. In addition, cortisol may play a role in stimulating hunger promoting neurotransmitters in the brain and decrease the activity of leptin (satiety hormone). In human, the stress response appears to stimulate appetite for high energy-dense foods.


What Helps With a Successful Weight Loss?

Healthy calorie restriction which eliminates the unhealthy sources and calorie dense foods, even in lean, healthy individuals, improves heart function, reduces inflammatory marker, reduces risk factors for cardiovascular disease such as LDL-C, triglycerides, and blood pressure, and reduces diabetes risk factors. Eating for a healthy life requires to combine calorie restriction and nutrient supplementation to be beneficial.

Studies of 4 popular diet plans all were found to be on average only 43.5% sufficient in Recommended Daily Intakes (RDIs) for 27 essential micronutrients values, and deficient in 15 of them.

Physical activity is required to maintain a healthy energy balance. It increases energy expenditure, and reduces appetite for short period of time, or by helping the body’s sensitivity to appetite controlling hormones like cholecystokin. It improves insulin resistance, metabolism and mood. Moderate exercise prevents muscle loss.

Enhancing the body's resting metabolism (REE), by using natural and plant based energy and metabolism boosters helps with weight loss. Guarana fruit (Paullinia cupana) seed extract has traditionally been used as a stimulant containing about 6% caffeine. Caffeine or guaranine from guarana, can help stimulate fat burning and improve metabolic rate. Guarana contains Saponins and polyphenols with other bioactive properties. At higher concentrations, Guarana extract may cause caffeine overdose symptoms and will not be beneficial anymore. Thus it should be consumed at the dose which is supported by the studies and from a high quality source.

Green tea polyphenols provide anti-inflammatory, antioxidant, and cholesterol-lowering, and modest weight loss effects in human studies. Green tea consumption for 12–13 weeks helped to decrease body weight by about 3 pounds compared to control group.

Improving the fat cell signaling system contributes to better success in weight management. Irvingia gabonensis is a mango-like fruit and its seeds' extracts have been shown to help reduce fat stores and to promote healthy blood lipid and fasting blood glucose levels. Irvingia gabonensis seed extract may help inhibiting adipogenesis (fat accumulation in fat cells) by down-regulating a protein that participates in activating fat cell growth and proliferation. Randomized controlled trials suggest Irvingia gabonensis seed extract contributed to lower body fat stores, weight, waist circumference, LDL cholesterol, Inflammatory marker (CRP), fasting blood sugar for those healthy overweight and/or obese volunteers taking 150 mg of Irvingia gabonensis seed extract before meals for 10 weeks compared to control group.

Keeping a healthy level of serotonin play an important role in healthy weight management. Amino acid Tryptophan is a precursor to serotonin. Lower brain's serotonin levels stimulate the desire to eat, while Increased brain serotonin levels promote satiety signal. This is in particular very important for those on diet, as the food elimination causes stress and deficiency in tryptophan, these individuals usually can't maintain their diet and when stop often put on more weight.

Limiting carbohydrates in the diet, and controlling their absorption contributes to maintaining a healthy weight. Of course, not all carbohydrates are bad. Carbohydrates include sugar, starch, Sugar alcohol( Xylitol, and moltitol) and Cellulose (fibre).

Carbohydrate in processed foods or refined foods made from plants, including sweets, cookies and candy, table sugar, honey, soft drinks, breads and crackers, jams and fruit products, pastas and breakfast cereals are all consist of high calorie that can be absorbed as sugar and stored by our body. Lower amounts of carbohydrate are usually associated with unrefined foods, including beans, tubers, and rice. Xylitol is naturally occurring in small amounts in plums, strawberries, cauliflower, and pumpkin and it has negligible effects on blood sugar, because it is metabolized independently of glucose regulating hormones.

The simple vs. complex distinction has little value for determining the nutritional quality of carbohydrates. Some simpler carbohydrates such as xylitol does not impact the blood sugar level. While some complex carbohydrates such as starches, especially if processed, raise blood sugar rapidly, fibre forms are hard to digest and actually help to lower blood sugar and cholesterol.

Extracts from kelp (Ascophyllum nodosum) and bladderwrack (Fucus vesiculosus) contribute to lowering the activity of the digestive enzymes alpha-amylase (α-amylase) and alpha-glucosidase (α-glucosidase) required for digesting dietary starches and therefore may reduce or slow the absorption of high glycemic carbohydrates. When taken just before a meal containing 50 grams of carbohydrates, 500 mg of the seaweed extract resulted in 12.1% reduction in insulin production and a 7.9% increase in its sensitivity compared to placebo group.

White kidney bean extract (Phaseolus vulgaris) contains an inhibitor of α-amylase as well. By inhibiting α-amylase, absorption of starch from the diet is reduced. Results from studies are suggesting that it helps with weight management, reducing blood triglycerides, and post meal glucose spike over time.

L-arabinose is hardly digested and absorbed in the intestine. L-arabinose is an indigestible plant compound, cannot be absorbed into the blood. For it to be utilized, requires enzyme sucrase. In this way, L-arabinose actually competes with sucrose sugars for the availability of the sucrase enzyme; therefore there will be less enzyme available to digest and absorb sucrose. In animal, L-arabinose prevented the rise in blood sugar following administration of sucrose. It has been also safe for both short- and long-term studies, and may contribute to lower levels of hemoglobin A1C.

Chromium. Chromium is an essential trace mineral and its a cofactor to insulin. Chromium contributes to insulin activity and play a role in maintaining healthy blood glucose levels.

Magnesium deficiency has been liked to increased risk of metabolic syndrome and diabetes. It has been shown to be able to decrease fasting insulin concentrations and it may also contribute to enhance satiety.

A critical enzyme called adenosine monophosphate-activated protein kinase (AMPK) is known as metabolic master switch due to its contribution to various aspects of metabolism. AMPK impacts the sugar metabolism and fat build up. AMPK activation may help protects against obesity and metabolic syndrome. The beneficial impacts of intense short exercise has been liked to activation of this enzyme. AMPK activation is also has been improved by certain nutritional compounds such as Hesperidin. Hesperidin belongs to the group of flavonoids, and after being digested it is metabolized to a compound called hesperetin along with other metabolites. Hesperetin provides antioxidant and anti-inflammatory, insulin-sensitizing, and lipid-lowering properties, also activates the AMPK pathway. Results from human clinical trials suggests taking 500 - 600mg of Hesperidin daily over 1-3 months produce those beneficial results.

Lipase enzyme helps with absorption of dietary fats. Reducing the activity of the lipase enzyme may reduce the total amount of dietary fat absorbed. The epigallocatechin gallate (EGCG) catechin antioxidant from green tea interferes with the activity of lipase. In animal studies it helped to lower LDL, visceral fat and body fat within 16 weeks.

Maintaining a healthy body weight is one of the key factors to a healthy long life. Obesity and excess body weight is responsible for many disease conditions such as chronic inflammation, Insulin resistance, Diabetes type 2, Cardiovascular diseases, High blood pressure, Arthritis, Joint pain, Indigestion, and even malignancies. New research suggests, eating less and dieting has will not provide a long lasting outcome for many individuals and actually may cause more harm and deficiency. Healthy weight loss requires a life style change along with addressing the underlying contributing physiological, psychological, poor nutrition conditions which could derived from poor habits as well as fad diets traps.

Articles and products featured by Health Palace are collected from a variety of sources and are provided as a service by Health Palace. These newsletters, while of potential interest to readers, do not necessarily represent the opinions nor constitute the advice of Health Palace. Presented materials are only for information purposes and do not intent to treat, cure, or prevent any disease.

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References:

  1. Hagobian, T. A., and Braun, B. Physical activity and hormonal regulation of appetite: sex differences and weight control. Exerc Sport Sci Rev. 2010;38(1):25–30.
  2. Aoki Y, Belin RM, Clickner R, Jeffries R, Phillips L, and Mahaffey KR. Serum TSH and total T4 in the United States population and their association with participant characteristics: National Health and Nutrition Examination Survey (NHANES 1999-2002). Thyroid. 2007;17(12):1211–23.
  3. Asvold, B. O., Bjøro, T., and Vatten, L. J. Association of serum TSH with high body mass differs between smokers and never-smokers. J Clin Endocrinol Metab. 2009;94(12):5023–7.
  4. Biondi, B. Thyroid and obesity: an intriguing relationship. J Clin Endocrinol Metab. 2010;95(8):3614–7.
  5. De Vriendt, T., Moreno, L. A., and De Henauw, S. Chronic stress and obesity in adolescents: scientific evidence and methodological issues for epidemiological research. Nutr Metab Cardiovasc Dis. 2009;19(7):511–9.
  6. Hill, J. O., Wyatt, H. R., and Peters, J. C. Energy balance and obesity. Circulation. 2012;126(1):126–32.
  7. King, N. A., Horner, K., Hills, A. P., et al. Exercise, appetite and weight management: understanding the compensatory responses in eating behaviour and how they contribute to variability in exercise-induced weight loss. Br J Sports Med. 2012;46(5):315–22.
  8. Kaufman, J. M., and Vermeulen, A. The decline of androgen levels in elderly men and its clinical and therapeutic implications. Endocr. Rev. 2005;26(6):833–76.
  9. Paolisso, G., Tagliamonte, M. R., Rizzo, M. R., and Giugliano, D. Advancing age and insulin resistance: new facts about an ancient history. Eur J Clin Invest. 1999;29(9):758–69
  10. Knutson KL, Spiegel K, Penev P, Van Cauter E. The metabolic consequences of sleep deprivation. Sleep medicine reviews. Jun 2007;11(3):163-178. 
  11. Lam, D. D., Garfield, A. S., Marston, O. J., Shaw, J., and Heisler, L. K. Brain serotonin system in the coordination of food intake and body weight. Pharmacology, Biochemistry and Behavior. 2010;97(1):84–91.
  12. Mayes, J. S., and Watson, G. H. Direct effects of sex steroid hormones on adipose tissues and obesity. Obes Rev. 2004;5(4):197–216.
  13. Myers MG Jr, Leibel RL, Seeley RJ, et al. Obesity and leptin resistance: distinguishing cause from effect. Trends Endocrinol Metab. 2010;21(11):643-51.
  14. Carbohydrates The Nutrition Source. Harvard School of Public Health. Retrieved April 3, 2013.
  15. Calton, J. B. Prevalence of micronutrient deficiency in popular diet plans. J Int Soc Sports Nutr. 2010;7:24.
  16. Bosy-Westphal A, Eichhorn C, Kutzner D, Illner K, Heller M, Muller MJ. The age-related decline in resting energy expenditure in humans is due to the loss of fat-free mass and to alterations in its metabolically active components. The Journal of nutrition. Jul 2003;133(7):2356-2362. 
  17. Krewer Cda C, Ribeiro EE, Ribeiro EA, et al. Habitual intake of guarana and metabolic morbidities: an epidemiological study of an elderly Amazonian population. Phytotherapy research: PTR.Sep 2011;25(9):1367-1374.
  18. Moustakas D, Mezzio M, Rodriguez BR, Constable MA, Mulligan ME, Voura EB. Guarana provides additional stimulation over caffeine alone in the planarian model. PloS one.2015;10(4):e0123310.
  19. Bose M, Lambert JD, Ju J, Reuhl KR, Shapses SA, Yang CS. The major green tea polyphenol, (-)-epigallocatechin-3-gallate, inhibits obesity, metabolic syndrome, and fatty liver disease in high-fat-fed mice. The Journal of nutrition. Sep 2008;138(9):1677-1683. 
  20. Chantre P, Lairon D. Recent findings of green tea extract AR25 (Exolise) and its activity for the treatment of obesity. Phytomedicine : international journal of phytotherapy and phytopharmacology. Jan 2002;9(1):3-8. 
  21. Hursel, R., Viechtbauer, W., and Westerterp-Plantenga, M. S. The effects of green tea on weight loss and weight maintenance: a meta-analysis. Int J Obes (Lond). 2009;33(9):956–61.
  22. Hursel R, Westerterp-Plantenga MS. Catechin- and caffeine-rich teas for control of body weight in humans. The American journal of clinical nutrition.Dec 2013;98(6 Suppl):1682s-1693s.
  23. Johnson, R., Bryant, S., and Huntley, A. L. Green tea and green tea catechin extracts: An overview of the clinical evidence. Maturitas. 2012 Dec;73(4):280-7.
  24. Juhel C, Armand M, Pafumi Y, Rosier C, Vandermander J, Lairon D. Green tea extract (AR25) inhibits lipolysis of triglycerides in gastric and duodenal medium in vitro. The Journal of nutritional biochemistry. Jan 2000;11(1):45-51.
  25. Koo SI, Noh SK. Green tea as inhibitor of the intestinal absorption of lipids: potential mechanism for its lipid-lowering effect. The Journal of nutritional biochemistry. Mar 2007;18(3):179-183.
  26. Breum L, Rasmussen MH, Hilsted J, Fernstrom JD. Twenty-four-hour plasma tryptophan concentrations and ratios are below normal in obese subjects and are not normalized by substantial weight reduction. The American journal of clinical nutrition. May 2003;77(5):1112-1118. 
  27. Cavaliere, H., and Medeiros-Neto, G. The anorectic effect of increasing doses of L-tryptophan in obese patients. Eat Weight Disord. 1997 Dec;2(4):211-5.
  28. Hrboticky, N., Leiter, L. A., and Anderson, G. H. Effects of L-tryptophan on short term food intake in lean men. Nutrition Research. 1985;5(6):595–607. 
  29. Barrett, M. L., and Udani, J. K. A proprietary alpha-amylase inhibitor from white bean (Phaseolus vulgaris): a review of clinical studies on weight loss and glycemic control. Nutr J. 2011;10:24.
  30. O’Neill HM, Maarbjerg SJ, Crane JD, et al. AMP-activated protein kinase (AMPK) beta1beta2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise. Proc Natl Acad Sci USA. 2011 Sep 20;108(38):16092-7.
  31. Chacko, S. A., Sul, J., Song, Y., et al. Magnesium supplementation, metabolic and inflammatory markers, and global genomic and proteomic profiling: a randomized, double-blind, controlled, crossover trial in overweight individuals. American Journal of Clinical Nutrition. 2011;93(2):463–73.
  32. Ngondi, J. L., Oben, J. E., and Minka, S. R. The effect of Irvingia gabonensis seeds on body weight and blood lipids of obese subjects in Cameroon. Lipids Health Dis. 2005;4:12
  33. Nguyen, N. T., Magno, C. P., Lane, K. T., Hinojosa, M. W., and Lane, J. S. Association of hypertension, diabetes, dyslipidemia, and metabolic syndrome with obesity: findings from the National Health and Nutrition Examination Survey, 1999 to 2004. J. Am. Coll. Surg. 2008;207(6):928–34.
  34. Ngondi JL, Etoundi BC, Nyangono CB, Mbofung CM, Oben JE. IGOB131, a novel seed extract of the West African plant Irvingia gabonensis, significantly reduces body weight and improves metabolic parameters in overweight humans in a randomized double-blind placebo controlled investigation. Lipids in health and disease. 2009;8:7. 
  35. Paradis, M.-E., Couture, P., and Lamarche, B. A randomised crossover placebo-controlled trial investigating the effect of brown seaweed (Ascophyllum nodosum and Fucus vesiculosus) on postchallenge plasma glucose and insulin levels in men and women. Appl Physiol Nutr Metab. 2011;36(6):913–9
  36. Haidari F, Heybar H, Jalali MT, Ahmadi Engali K, Helli B, Shirbeigi E. Hesperidin supplementation modulates inflammatory responses following myocardial infarction. Journal of the American College of Nutrition. 2015;34(3):205-211.
  37. Hooper, L., Kroon, P. A., Rimm, E. B., et al. Flavonoids, flavonoid-rich foods, and cardiovascular risk: a meta-analysis of randomized controlled trials. American Journal of Clinical Nutrition. 2008;88(1):38–50
  38. Homayouni F, Haidari F, Hedayati M, Zakerkish M, Ahmadi K. Hesperidin Supplementation Alleviates Oxidative DNA Damage and Lipid Peroxidation in Type 2 Diabetes: A Randomized Double-Blind Placebo-Controlled Clinical Trial. Phytotherapy research : PTR. Aug 14 2017.
  39. Li C, Schluesener H. Health-promoting effects of the citrus flavanone hesperidin. Critical reviews in food science and nutrition. Feb 11 2017;57(3):613-631.
  40. Benedict C, Brooks SJ, O'Daly OG, Almen MS, Morell A, Aberg K, . . . Schioth HB. Acute sleep deprivation enhances the brain's response to hedonic food stimuli: an fMRI study. The Journal of clinical endocrinology and metabolism. Mar 2012;97(3):E443-447. 
  41. Bastard, J.-P., Maachi, M., Lagathu, C., et al. Recent advances in the relationship between obesity, inflammation, and insulin resistance. Eur. Cytokine Netw. 2006;17(1):4–12.
  42. Andersen T, Fogh J. Weight loss and delayed gastric emptying following a South American herbal preparation in overweight patients. Journal of human nutrition and dietetics: the official journal of the British Dietetic Association.Jun 2001;14(3):243-250.
  43. Aleksandrova K, Nimptsch K, Pischon T. Obesity and colorectal cancer. Frontiers in bioscience. 2013;5:61-77.
  44. Allott EH, Masko EM, Freedland SJ. Obesity and Prostate Cancer: Weighing the Evidence. European urology. Nov 15 2012.
  45. Hampel, H., Abraham, N. S., and El-Serag, H. B. Meta-analysis: obesity and the risk for gastroesophageal reflux disease and its complications. Ann Intern Med. 2005;143(3):199–211

12th Jan 2019

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