Melatonin is a hormone that is naturally produced by the pineal gland in the brain. Its main job is to help regulate the body’s circadian rhythms, which are the natural cycles of sleeping and waking that occur daily. Melatonin is particularly important for getting a good night’s sleep, and it can also have positive effects on overall health and weight.
One of the key functions of melatonin is to help regulate the sleep-wake cycle. When it gets dark outside, the body naturally begins to produce more melatonin, which signals to the brain that it’s time to wind down and prepare for sleep. Conversely, when it gets light outside, melatonin production decreases, which tells the brain that it’s time to wake up and start the day. By regulating these cycles, melatonin can help improve sleep quality and ensure that people wake up feeling refreshed and ready to tackle the day.
In addition to its effects on sleep, melatonin has also been shown to have a number of other health benefits. For example, it is a potent antioxidant, meaning that it can help protect cells from damage caused by harmful molecules called free radicals. This can in turn help reduce the risk of a number of different diseases, including cancer and cardiovascular disease.
Melatonin has also been shown to have positive effects on weight management. In one study, researchers found that supplementing with melatonin helped to reduce body weight and fat mass in overweight and obese individuals. The researchers speculated that this may be due to the fact that melatonin can help improve sleep quality, which in turn can lead to changes in appetite and energy levels.
Overall, it is clear that melatonin is an important hormone that can have positive effects on both sleep and overall health. If you are struggling to get a good night’s sleep, or if you are interested in improving your overall wellbeing, consider talking to a functional nutritionist about incorporating melatonin into your daily routine.
References:
Godfrey, D. A. (2017). Melatonin as a therapeutic intervention in otolaryngology: Head and neck surgery. Sleep Science and Practice, 1(1).
Pires, W., & Bordini, E. A. (2019). The effects of melatonin on weight gain, fat mass, and lipid metabolism: a systematic review. Frontiers in Endocrinology, 10, 86.
Vollmer, C., Michel, U., & Randler, C. (2012). Outdoor light at night (LAN) is correlated with eveningness in adolescents. Chronobiology International, 29(4), 502-508.
Leptin is a hormone produced by our fat cells that regulates how much we eat and the amount of energy we burn. Its main function is to signal the brain when we have eaten enough and are satiated, thus promoting weight loss. However, sometimes the body becomes resistant to the effects of leptin, and this can lead to overeating and weight gain. This condition is known as leptin resistance.
Leptin resistance occurs when the body stops responding to the signal produced by the hormone. This can happen due to a number of reasons, but the most common is excess body fat. Excessive amounts of fat in the body lead to a constant release of leptin, and over time the brain becomes desensitized to the signal. When this happens, the body thinks it’s starving and sends signals to increase appetite and store more fat, leading to weight gain.
There are other factors that contribute to the development of leptin resistance such as poor diet, lack of exercise, poor sleep, and high-stress levels. A diet high in sugar, processed foods, and saturated fats has been shown to increase inflammation levels in the body, which can affect how leptin is produced and how it functions.
Another factor that contributes to leptin resistance is lack of sleep. Poor sleep can affect the production of leptin, making it difficult for the body to regulate food intake and energy expenditure properly.
The good news is that leptin resistance is reversible. By maintaining a healthy diet and exercise routine, and reducing stress levels, you can gradually reduce the amount of fat in your body and restore proper leptin function. Studies have shown that consuming a high-fiber, low-fat diet can help reduce inflammation levels and promote weight loss, therefore improving leptin sensitivity.
Other interventions that can improve the body’s response to leptin include getting enough sleep, reducing stress levels through yoga or meditation practices, and starting a regular exercise routine. Resistance training, in particular, has been shown to be effective in improving the function of leptin.
In conclusion, leptin resistance is a condition that contributes significantly to overweight and obesity, and its prevalence continues to increase worldwide. Therefore, it is important to understand its causes and how to mitigate them. Maintaining a healthy diet, getting enough sleep, exercising regularly, and managing stress levels are ways by which you can address leptin resistance and achieve your weight loss goals.
References:
Rosenbaum M, Leibel RL. Role of energy expenditure in the development of leptin resistance. J Clin Invest. 2014;124(2): 420-2.
Juge-Aubry CE, Henrichot E, Meier CA. Adipose tissue: a regulator of inflammation. Best Pract Res Clin Endocrinol Metab. 2005;19(4):547-566.
Halpern B, Mancini MC. Leptin reduction and its interactions with diabetes control after bilio-pancreatic diversion. Surg Obes Relat Dis. 2009;5(1):48-53.
Lopez-Jaramillo P, Gomez-Arbelaez D, Lopez-Lopez J, Lombana-Rodriguez HA, Paez-Canro C, Rueda-Quijano SM, et al. The role of leptin/adiponectin ratio in metabolic syndrome and diabetes. Horm Mol Biol Clin Investig.[Internet] 2014;19(3):167-176. Available from: http://www.ncbi.nlm.nih.gov/pubmed/25403381
Consitt LA, Saxena G. Exercise training and insulin resistance: a current review. J Obes.[Internet] 2013;2013: Vaiycn858690. Available from: https://www.ncbi.nlm.nih.gov/pubmed/23533342
Vitamin D is a fat-soluble secosteroids. There are two main forms of vitamin D: vitamin D2, also called ergocalciferol, and vitamin D3, also called cholecalciferol. Scientific studies suggest that cholecalciferol is the more effective form of the vitamin. Vitamin D2 is obtained exclusively from the diet and comes mostly from fortified foods and plants like mushrooms grown in UV lights. Vitamin D3 is found in animal foods like oily fish and fish oil, liver, egg yolks and butter. Our skin also manufactures vitamin D3 upon exposure to light.
The Primary Types of Vitamin D and How They Interact With The Body
Specifically, vitamin D3 originates from a compound found in the skin called 7-dihydroxycholesterol when exposed to sunlight, particularly UV-B light. Vitamin D production is complex and involves metabolic processes that take place in the liver and the kidneys. In the liver, vitamin D2 and D3 undergo hydroxylation in the presence of mitochondrial and microsomal hydroxylase producing 25-hydroxyvitamin D (25(OH)D), also referred to as calcidiol. This is further metabolized in the kidneys to produce calcitriol (1,25(OH)2D). To determine the amount of serum vitamin D, one measures 25(OH)D biomarker with a half-life of around 2 to 3 weeks.
Vitamin D plays an important role in bone health, calcium homeostasis and the immune system as well as the cardiovascular and endocrine systems. Vitamin D deficiency is also associated with type-2 diabetes, Alzheimer’s disease, osteoporosis, Parkinson’s disease, and cancer. Recent studies have shown that at least 20 types of cancers are associated with low serum vitamin D.
Vitamin D and The Mammary Glands
A recent review aimed at studying the connection between vitamin D deficiency and breast cancer revealed a correlation between increased breast cancer risk and vitamin D receptor genetic polymorphism (VDR). VDR genes regulate hormone differentiation, milk production, and calcium transport during lactation in the mammary glands. Data from two randomized clinical trials show that women with higher concentrations of vitamin D (>60 ng/ml) had 82% lower incidence rate of breast cancer than women with lower concentrations of vitamin D (<20 ng/ml). A comparison with the healthy controls indicated a significant risk of breast cancer to women with vitamin D levels less than 20ng/ml developed metastases, and 73% died due to the advanced illness.
Reference
Atoum M, Alzoughool F. Vitamin d and breast cancer: latest evidence and future steps. Breast Cancer (Auckl). 2017 Jan;11:117822341774981.
Folate, Vitamin B12, Vitamin B6, Choline
What is the significance of each of your four vitamins? What roles do they play in the body? What bodily systems are affected?
What is the RDA level for each of the vitamins? What is the upper limit for each of the vitamins? What are the signs or symptoms of deficiency and toxicity for each of the vitamins?
Where are these vitamins found in the diet and what may impede availability and absorption? How does the concept of food poverty impact a client’s ability to obtain these vitamins? (For more information on food poverty, click this link Sustain.
The scientific community is still in disagreement as to whether or not obesity is a disease. While some still consider obesity a self-inflicted disease caused by poor eating habits and lack of exercise, there is growing evidence to support the claim that obesity is a disease.
According to Pi-Sunyer (2002), not only is obesity a disease but within the United States it is considered to be a condition of epidemic proportions. Statistics show that, in our country, over 20% of adults are diagnosed as clinically obese (Pi-Sunyer, 2002). The rationale that obesity is a disease is due to the fact that it causes many different comorbidities such as high blood pressure, diabetes, heart disease, etc.
Has Obseity Reached Epidemic Proportions In Western Countries?
I agree with Conway and Rene (2004) who believe that obesity is not only a condition that has reached epidemic proportions, but it is a disabling, multifaceted disease that causes changes in organ function and can come with a host of comorbidities. The excess body weight puts a strain on the heart, leading to changes in anatomical structure and the function of the organ. Obesity has also repercussions on the immune system (de Heredia et al., 2012), endocrine system (Poddar et al., 2017), and pulmonary system (Dixon & Peters, 2018). These repercussions are caused by both mechanical and functional alteration of tissues and organs.
Data Suggests That Obseity Is Associated With Several Very Serious Health Concerns
Research studies show that obesity is associated with an increased risk of developing cancer in at least 13 different organs (Avgerinos et al., 2019). Obesity is also linked to type-2 diabetes (Maggio & Pi-Sunyer, 2003), arthritis (Moroni et al., 2020). At the same time, a systematic review of scientific data that was published in 2017 shows that weight-loss interventions in the obese adult population decrease all-cause mortality (Ma et al., 2017). The same review shows that weight loss has a positive impact on cardiovascular mortality and cancer mortality (Ma et al., 2017).
Lastly, obesity’s status and acceptance as a disease are pivotal in determining its treatment, reimbursement for treatment, and the development of widespread interventions. For these reasons, I believe that obesity should be recognized as a disease.
References
Avgerinos, K. I., Spyrou, N., Mantzoros, C. S., & Dalamaga, M. (2019). Obesity and cancer risk: Emerging biological mechanisms and perspectives. Metabolism: clinical and experimental, 92, 121–135. https://doi.org/10.1016/j.metabol.2018.11.001
de Heredia, F. P., Gómez-Martínez, S., & Marcos, A. (2012). Obesity, inflammation and the immune system. The Proceedings of the Nutrition Society, 71(2), 332–338. https://doi.org/10.1017/S0029665112000092
Ma, C., Avenell, A., Bolland, M., Hudson, J., Stewart, F., Robertson, C., Sharma, P., Fraser, C., & MacLennan, G. (2017). Effects of weight loss interventions for adults who are obese on mortality, cardiovascular disease, and cancer: systematic review and meta-analysis. BMJ (Clinical research ed.), 359, j4849. https://doi.org/10.1136/bmj.j4849
Maggio, C. A., & Pi-Sunyer, F. X. (2003). Obesity and type 2 diabetes. Endocrinology and metabolism clinics of North America, 32(4), 805–viii. https://doi.org/10.1016/s0889-8529(03)00071-9
Moroni, L., Farina, N., & Dagna, L. (2020). Obesity and its role in the management of rheumatoid and psoriatic arthritis. Clinical rheumatology, 39(4), 1039–1047. https://doi.org/10.1007/s10067-020-04963-2
Pi-Sunyer, F. X. (2002). The obesity epidemic: Pathophysiology and consequences of obesity. Obesity Research, 10(S12), 97S-104S. https://doi.org/10.1038/oby.2002.202
Poddar, M., Chetty, Y., & Chetty, V. T. (2017). How does obesity affect the endocrine system? A narrative review. Clinical obesity, 7(3), 136–144. https://doi.org/10.1111/cob.12184
Gluten is a family of storage proteins found in wheat, rye, triticale, and barley. In predisposed individuals, ingestion of gluten causes disease reactions that are grouped under the term gluten-related disorders (GRD). Only a decade ago, GRD were rare in the United States, but the rate of gluten-related disorders has greatly increased since then. It is now estimated that GRD affect close to 10% of the population (Sapone et al., 2012).
There are five kinds of gluten-related disorders recognized by the medical community. Each disorder presents with unique pathophysiology and etiology. Celiac disease, dermatitis herpetiformis, and gluten ataxia are autoimmune conditions; wheat allergy is an allergic disease (Taraghikhah et al., 2020), and non-celiac gluten sensitivity is a non-autoimmune-allergic disease (Sharma et al, 2020).
Celiac Disease and Gluten
Celiac disease (CD) is a chronic, auto-immune condition that affects genetically predisposed individuals. It is thought that genetically predisposed individuals develop an immune response to unknown environmental factors which is then triggered by the ingestion of gluten (Lebwohl et al., 2018). CD can cause atrophy of the small intestinal villi, which leads to malabsorption, diarrhea, and failure to thrive. But manifestations of CD can also be minimal, like negligible mucosal lesions, or it can have an asymptomatic presentation, which often causes delayed diagnosis. Celiac disease can also present with extraintestinal manifestations ranging from neurologic disorders, psychiatric disorders, infertility, recurrent miscarriages, osteoporosis and osteopenia, arthritis, aphthous stomatitis (a disease my mother suffers from), dental enamel hypoplasia, and elevations in transaminases (Barker & Liu, 2008).
Dermatitis Herpetiformis and Gluten
Dermatitis Herpetiformis (DH), also known as Duhring-Brocq disease, is an auto-immune condition that affects the skin and causes chronic blistering and lesions. The lesions and blisters generally cover the areas of the scalp, knees, elbows, ankles, and buttocks, producing intense burning and itching. The skin of people affected by DH presents with the same protein IgA1 with J chain and secretory component found in the small intestinal mucosa in adult celiac disease, suggesting a strong correlation between the two conditions (Cohen et al., 1997). For this reason, DH is also called the “celiac disease of the skin”, and the European Society for Pediatric Gastroenterology, Hepatology and Nutrition now states that a dermatitis herpetiformis diagnosis confirms the celiac disease diagnosis without the need for intestinal biopsy. People affected by DH can suffer from various degrees of gastrointestinal issues that vary from milk lesions of the mucosal lining of the small intestine to villous atrophy (Mendez et al., 2013).
Gluten Ataxia as an Autoimmune
Gluten ataxia (GA) is an autoimmune disease triggered by the ingestion of gluten that affects primarily the cerebellum, the part of the brain responsible for coordination and movement. The cerebellum is also responsible for balance, eye movement, and the kind of motor learning abilities involved in learning movements that require practice and fine-tuning, for example, riding a bike or playing an instrument (Leopold, 2018). In GA, the immune system creates antibodies that attack and destroy the Purkinje cells, causing problems with vision and fine motor skills, gait abnormalities, and balance issues. It can also cause peripheral neuropathy, also known as gluten neuropathy (Hadjivassiliou et al., 2004). The damage to the Purkinje cells is irreversible, and studies involving brain MRIs show that up to 60% of subjects affected by GA suffer from permanent shrinkage of the cerebellum (Sapone et al., 2012).
Wheat Allergies and Gluten
Wheat allergy (WA) is an allergic reaction to gluten in which the immune system produces immunoglobulin E antibodies in response to wheat proteins. It can present with gastrointestinal symptoms similar to celiac disease, but unlike CD, WA has a fast onset. When inhaled (baker’s asthma), WA can cause asthma and rhinitis. When someone affected by WA touches wheat, skin reactions occur. When ingested, wheat causes gastrointestinal pain, diarrhea, malabsorption, and, if untreated, it can lead to failure to thrive. WA can also cause anaphylactic shock, but it does not cause villi atrophy (Elli et al., 2015).
Gluten Sensitivity
Non-celiac gluten sensitivity (NCGS) is a non-autoimmune-allergic disease that presents with gastrointestinal and/or extraintestinal symptoms similar to the ones seen in CD (altered bowel habits, skin rashes, bone pain, headaches, fatigue, and depression). Laboratory testing shows no serum antibodies, and intestinal biopsies do not show villous atrophy. This lack of biomarkers makes NCGS difficult to diagnose, and it also can lead to misdiagnosis. NCGS can be misdiagnosed as IBS, and oftentimes only a strict elimination diet allows for a conclusive diagnosis (Biesiekierski et al., 2011). Molina-Infante et al. (2014) estimate that the prevalence of NCGS is 6 to 10 times higher than CD and WA and that it is more prevalent in family members of CD sufferers.
References
Barker, J. M., & Liu, E. (2008). Celiac disease: pathophysiology, clinical manifestations, and associated autoimmune conditions. Advances in pediatrics, 55, 349–365. https://doi.org/10.1016/j.yapd.2008.07.001
Biesiekierski, J. R., Newnham, E. D., Irving, P. M., Barrett, J. S., Haines, M., Doecke, J. D., Shepherd, S. J., Muir, J. G., & Gibson, P. R. (2011). Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. The American journal of gastroenterology, 106(3), 508–515. https://doi.org/10.1038/ajg.2010.487
Cohen LM, Skopicki DK, Harrist TJ, Clark WHJ. Elder D, Elenitsas R, Jarsorsky C, Johnson BJ. Lever’s Histopathology of the Skin. 8. Raven: Lippincott; 1997. Noninfectious Vesiculobullous and Vesiculopustular Diseases; pp. 209–252.
Elli, L., Branchi, F., Tomba, C., Villalta, D., Norsa, L., Ferretti, F., Roncoroni, L., & Bardella, M. T. (2015). Diagnosis of gluten related disorders: Celiac disease, wheat allergy and non-celiac gluten sensitivity. World journal of gastroenterology, 21(23), 7110–7119. https://doi.org/10.3748/wjg.v21.i23.7110
Hadjivassiliou, M., Williamson, C. A., & Woodroofe, N. (2004). The immunology of gluten sensitivity: beyond the gut. Trends in Immunology, 25(11), 578–582. https://doi.org/10.1016/j.it.2004.08.011
Mendes, F. B., Hissa-Elian, A., Abreu, M. A., & Gonçalves, V. S. (2013). Review: dermatitis herpetiformis. Anais brasileiros de dermatologia, 88(4), 594–599. https://doi.org/10.1590/abd1806-4841.20131775
Molina-Infante, J., Santolaria, S., Montoro, M., Esteve, M., & Fernández-Bañares, F. (2014). Sensibilidad al gluten no celiaca: una revisión crítica de la evidencia actual [Non-celiac gluten sensitivity: a critical review of current evidence]. Gastroenterologia y hepatologia, 37(6), 362–371. https://doi.org/10.1016/j.gastrohep.2014.01.005
Sapone, A., Bai, J. C., Ciacci, C., Dolinsek, J., Green, P. H., Hadjivassiliou, M., Kaukinen, K., Rostami, K., Sanders, D. S., Schumann, M., Ullrich, R., Villalta, D., Volta, U., Catassi, C., & Fasano, A. (2012). Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC medicine, 10, 13. https://doi.org/10.1186/1741-7015-10-13
Sharma, N., Bhatia, S., Chunduri, V., Kaur, S., Sharma, S., Kapoor, P., Kumari, A., & Garg, M. (2020). Pathogenesis of Celiac Disease and Other Gluten Related Disorders in Wheat and Strategies for Mitigating Them. Frontiers in Nutrition, 7. https://doi.org/10.3389/fnut.2020.00006
Taraghikhah, N., Ashtari, S., Asri, N., Shahbazkhani, B., Al-Dulaimi, D., Rostami-Nejad, M., Rezaei-Tavirani, M., Razzaghi, M. R., & Zali, M. R. (2020). An updated overview of spectrum of gluten-related disorders: clinical and diagnostic aspects. BMC Gastroenterology, 20(1). https://doi.org/10.1186/s12876-020-01390-0
Our total daily energy expenditure (TDEE) is dictated by three factors: resting metabolic rate (RMR), which is the number of calories our body needs to perform metabolic functions when it is at rest; the number of calories burnt through physical activity, non-exercise activity thermogenesis (NEAT), and exercise; and the number of calories needed to digest and absorb food. This is called diet-induced thermogenesis (DIT) or thermal effect of feeding (TEF).
Total daily energy expenditure varies from individual to individual and across age, sex, total body weight, physical activity, percentage of fat free mass (FFM), also called lean body mass, versus fat mass (FM), as well as hormones; all play a role in TDEE. In general, RMR accounts for 60% of TDEE, physical activity account for 25-35% of TDEE, and DIT accounts for 5-15% of total energy expenditure.
How Is Food Converted Into Usable Energy?
The foods and beverages that we consume are combined with oxygen and converted into energy in the form of ATP. They also provide the building blocks used to make hormones and enzymes to grow and repair tissue as well as many other processes. When we eat, digest and assimilate food we burn calories. Diet-induced thermogenesis begins immediately after we eat and can last several hours, depending on the macronutrient composition of the meal. The word thermogenesis comes from the Greek θερμός (thermos) and γένεση (genesis), and it means the creation of heat. Not only does DIT create heat during food digestion and absorption, but it also (by a mechanism still not completely understood) activates the sympathetic nervous system which causes the body to produce heat in brown adipose tissue (BAT). BAT is only stimulated by cold temperatures (shivering) and food consumption.
What Exactly Is A Calorie?
A calorie is a unit of energy. It would be simple to think that a calorie is a calorie and that, therefore, 100 calories of steak are the same as 100 calories of brownies, or butter, or broccoli. But different macronutrients require different amounts of ATP to be metabolized and stored. This is why different macronutrients have different thermogenic effects, and DIT can vary greatly depending on the macronutrient composition of our diet.
Protein and alcohol have the highest thermic effects. The DIT for protein is calculated to be between 20 to 30%; the DIT of alcohol is between 10 and 30%. The thermic effect of carbohydrates is between 5 and 10%, and fat has the lowest reported DIT: 0 to 3%. This means that given the same number of calories, meals rich in protein, fat, carbohydrate, or alcohol have different effect on energy expenditure.
Studies show that postprandial thermogenesis in healthy subjects is increased 100% on a high-protein/low-fat diet versus a high-carbohydrate/low-fat carbohydrate diet. In addition, compared to fats and carbohydrates, protein consumption also provides increased satiety. Satiety scores were higher during high protein/high carbohydrate meals versus high fat meals. For these reasons, high protein diets are favored for weight loss as well as for weight maintenance.
How Does Food Effect Metabolism?
When researching the effects of food on metabolism, the next logical question to address is the following: would eating many smaller meals burn more calories than eating one to two larger meals in a 24-hour period? I found contradicting studies when reviewing the literature. Some studies showed that nibbling throughout the day caused a greater caloric expenditure, while other studies showed that consuming larger meals was linked to greater caloric expenditure. It seems that when it comes to meal frequency and metabolism the jury is still out.
There are other nutrients that stimulate metabolism and cause thermogenesis without contributing any calories. These nutrients are caffeine, capsaicin, and cold water. Caffeine is an alkaloid found in coffee beans, tea leaves, and cocoa beans. It is a stimulant and studies show that a cup of coffee can boost metabolism by 3-11%. A study also showed that caffeine may affect lean people more than overweight people as fat burning in lean women increased by 29% with caffeine consumption but obese women registered an increase of only 10%. Capsaicin is a compound found in chili peppers that stimulates metabolism and helps reduce energy intake. Finally, consuming water increases metabolism by 10-30% for about an hour. Cold water may promote an even greater caloric expenditure, as the body uses extra energy to raise the water temperature to body temperature.
References:
Raben A, Agerholm-Larsen L, Flint A, Holst JJ, Astrup A. Meals with similar energy densities but rich in protein, fat, carbohydrate, or alcohol have different effects on energy expenditure and substrate metabolism but not on appetite and energy intake. Am J Clin Nutr. 2003 Jan;77(1):91–100.
Westerterp-Plantenga MS, Rolland V, Wilson SA, Westerterp KR. Satiety related to 24 h diet-induced thermogenesis during high protein/carbohydrate vs high fat diets measured in a respiration chamber. Eur J Clin Nutr. 1999 Jun;53(6):495–502.
Acheson KJ: Influence of autonomic nervous system on nutrient-induced thermogenesis in humans. Nutrition. 1993, 9 (4): 373-80.
Hermsdorff HHM, Volp ACP, Bressan J. [Macronutrient profile affects diet-induced thermogenesis and energy intake]. Arch Latinoam Nutr. 2007 Mar;57(1):33–42.
Jequier E. Thermogenic responses induced by nutrients in man: their importance in energy balance regulation. Experientia Suppl. 1983;44:26–44.
Scott CB, Devore R. Diet-induced thermogenesis: variations among three isocaloric meal-replacement shakes. Nutrition. 2005 Jul 1;21(7):874–7.
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