Obesity is a complex, multifactorial disease characterized by excessive body fat that increases the risk of other diseases and health issues. It is usually defined by a Body Mass Index (BMI) of 30 or higher. This article offers a systematic overview of obesity, including its causes, consequences, and strategies for prevention, management and MIT homeopathy treatment.
Obesity results from a combination of genetic, behavioral, metabolic, and hormonal influences on body weight. The primary cause is an energy imbalance between calories consumed and calories expended.
Genetics can play a significant role in obesity, affecting how one’s body processes food into energy and how fat is stored. A sedentary lifestyle and high-calorie diets rich in sugars and fats contribute significantly to obesity. Lack of access to healthy foods, high-stress environments, and marketing of unhealthy foods can influence eating behaviors. Emotional stress and certain mental health conditions like depression may lead to overeating as a coping mechanism.
The effects of obesity extend far beyond physical appearance, significantly impacting health and leading to a range of chronic conditions. Excess fat can lead to high blood pressure, abnormal cholesterol levels, and increased risk of coronary heart disease and stroke. Obesity is a major risk factor for type 2 diabetes by affecting how the body processes glucose. Being overweight or obese increases the risk of developing certain cancers, including breast, colon, and kidney cancer. Obesity can also affect mental health, leading to depression, anxiety, and low self-esteem.
Preventing and managing obesity requires a multi-faceted approach, including lifestyle modifications, medical interventions, and, in some cases, surgery. Incorporating a healthy diet and regular physical activity is essential for weight management. This includes eating more fruits, vegetables, lean proteins, and whole grains, and reducing sugar and saturated fat intake. For some, medications may be necessary to manage obesity, particularly if lifestyle changes have not been effective and if there are other health conditions. Bariatric surgery may be an option for people with severe obesity when other treatments have failed. It can lead to significant weight loss and help improve many obesity-related conditions.
Managing obesity is challenging, requiring sustained effort and support. Future strategies may include more personalized approaches to treatment, taking into account an individual’s genetic background, lifestyle, and the environment they live in. There is also an increasing emphasis on public health policies to create environments that support healthy living.
PATHOPHYSIOLOGY OF OBESITY
The pathophysiology of obesity involves complex interactions between genetic, environmental, and lifestyle factors that lead to an imbalance between energy intake and energy expenditure. This imbalance ultimately results in the accumulation of excess body fat.
Certain genes are associated with obesity, affecting appetite, metabolism, fat storage, and the distribution of body fat. These genes can influence how efficiently the body converts food into energy and how it stores excess calories.
At the core of obesity is an energy imbalance where caloric intake exceeds caloric expenditure. This can be due to overeating, consuming high-calorie, nutrient-poor foods, and leading a sedentary lifestyle.
Individuals with obesity may have a lower BMR, meaning they burn fewer calories at rest, contributing to weight gain over time.
Obesity is associated with changes in insulin sensitivity, leading to insulin resistance. This condition impairs glucose uptake by cells, contributing to high blood sugar levels and promoting fat storage.
Leptin is a hormone produced by fat cells that signals satiety to the brain. In obesity, the effectiveness of leptin signaling is reduced (leptin resistance), leading to increased appetite and food intake. Ghrelin is known as the “hunger hormone” because it stimulates appetite. Levels of ghrelin might not decrease as much after eating in individuals with obesity, leading to increased food intake.
Diets high in calories, sugars, and fats contribute to the development of obesity. Sedentary lifestyles reduce the amount of energy expended, contributing to energy imbalance and weight gain. Lack of sleep is linked to hormonal changes that increase appetite and cravings for high-calorie foods. Stress and emotional distress can lead to increased intake of high-calorie “comfort foods” that contribute to weight gain.
In obesity, adipocytes (fat cells) undergo hypertrophy (increase in size) and hyperplasia (increase in number), leading to adipose tissue dysfunction. This dysfunction can cause inflammation and the release of pro-inflammatory cytokines, contributing to systemic inflammation and insulin resistance.
The pathophysiology of obesity is multifactorial, involving a complex interplay between genetic, metabolic, hormonal, environmental, and psychological factors. Understanding these mechanisms is crucial for developing effective prevention and treatment strategies for obesity and its related health conditions.
ENZYME PATHWAYS INVOLVED IN OBESITY
The development and maintenance of obesity involve various biological pathways, including those governed by enzymes that regulate metabolism, energy storage, and appetite. Some of these enzymes play crucial roles in the synthesis and breakdown of lipids, proteins, and carbohydrates, impacting body weight and composition. Here’s an overview of key enzymes involved in obesity, along with their known activators and inhibitors:
Lipoprotein Lipase (LPL) is essential for the hydrolysis of triglycerides in lipoproteins into free fatty acids, which are then taken up by tissues for energy use or storage. Insulin activates LPL, particularly in adipose tissue, facilitating fat storage. Niacin (nicotinic acid) and some fish oils can inhibit LPL activity, reducing fat storage in adipose tissue.
Hormone-Sensitive Lipase (HSL) is responsible for the breakdown of stored triglycerides in adipocytes into free fatty acids and glycerol, releasing them into the bloodstream for energy. Catecholamines (e.g., adrenaline) and glucagon activate HSL, promoting lipolysis. Insulin inhibits HSL activity, reducing the mobilization of stored fats.
Adiponectin, though not an enzyme itself, influences various metabolic processes, including fatty acid oxidation and glucose regulation. It enhances the body’s sensitivity to insulin. Weight loss, physical exercise, and certain dietary components (e.g., omega-3 fatty acids) can increase adiponectin levels. Obesity is associated with reduced levels of adiponectin, contributing to insulin resistance.
Acetyl-CoA Carboxylase (ACC) plays a crucial role in fatty acid synthesis by converting acetyl-CoA to malonyl-CoA, a building block for new fatty acids. Insulin activates ACC, promoting lipogenesis (fat synthesis). AMP-activated protein kinase (AMPK) inhibits ACC, reducing fatty acid synthesis and promoting fatty acid oxidation.
Fatty Acid Synthase (FAS) is involved in the synthesis of long-chain fatty acids from acetyl-CoA and malonyl-CoA. Carbohydrate intake can activate FAS through increased levels of malonyl-CoA. Polyunsaturated fatty acids (PUFAs) and certain phytochemicals can inhibit FAS, reducing fatty acid synthesis.
AMP-Activated Protein Kinase (AMPK) is a key regulator of energy balance, activating energy-producing pathways (like glucose uptake and fatty acid oxidation) and deactivating energy-consuming processes (like lipogenesis). Exercise and various pharmacological agents, including metformin, can activate AMPK. High levels of ATP (energy currency of the cell) inhibit AMPK, signaling abundant energy availability.
Ghrelin O-Acyltransferase (GOAT) activates ghrelin (hunger hormone), influencing appetite and energy balance. Fasting or energy deficit increases ghrelin acylation by GOAT, stimulating hunger. Certain peptides and compounds are being researched for their potential to inhibit GOAT, aiming to reduce appetite and food intake.
Understanding the role of these enzymes and their regulation offers potential therapeutic targets for managing obesity. However, it’s important to recognize that the regulation of body weight is incredibly complex, involving not only these enzymes but also numerous hormonal and neurological pathways.
ROLE OF ENDOCRINE SYSTEM IN OBESITY
Hormones play a pivotal role in regulating metabolism, appetite, fat distribution, and energy storage, thus significantly influencing the development and progression of obesity. Here’s an overview of key hormones involved in obesity and their functions:
Insulin, secreted by the pancreas, helps control blood glucose levels by facilitating the uptake of glucose into cells and inhibiting glucose production in the liver. It also plays a critical role in fat storage. High levels of insulin (hyperinsulinemia) are often associated with obesity. Insulin resistance, a condition where cells fail to respond to insulin effectively, is common in obesity and can lead to type 2 diabetes.
Leptin, a hormone produced by fat cells, signals the brain to regulate energy balance by inhibiting hunger, which in turn diminishes fat storage in adipocytes. Despite high levels of leptin in obese individuals, many experience leptin resistance, where the brain does not respond to leptin signals, leading to increased food intake and reduced energy expenditure.
Ghrelin, known as the “hunger hormone,” is produced in the stomach and stimulates appetite, increasing food intake and promoting fat storage. Levels of ghrelin typically decrease after eating in healthy individuals. However, in those with obesity, ghrelin levels might not decrease as much, potentially leading to increased food intake.
Adiponectin, released by fat cells, enhances sensitivity to insulin, regulates glucose levels, and fatty acid breakdown. Lower levels of adiponectin are found in individuals with obesity, contributing to insulin resistance and metabolic syndrome.
Cortisol is a steroid hormone released in response to stress and low blood-glucose concentration. It supports fat storage and can influence where fat is stored in the body. Chronic stress can lead to elevated cortisol levels, promoting abdominal fat accumulation, which is associated with a higher risk of cardiovascular disease and diabetes.
Thyroid hormones regulate metabolism, with impacts on energy balance and weight. They influence how fast or slow the organs should work. Hypothyroidism (low thyroid hormone levels) can reduce metabolism, leading to weight gain. However, obesity itself can also affect thyroid function.
Estrogens and androgens (including testosterone) influence body fat distribution and muscle mass. Hormonal imbalances can affect body composition and fat distribution, contributing to obesity. For example, low testosterone levels in men and high androgen levels in women (as seen in polycystic ovary syndrome) can contribute to weight gain.
The hormones involved in obesity interact in complex networks, influencing appetite, metabolism, and fat distribution. This intricate hormonal interplay highlights the complexity of obesity as a disease, going beyond simple caloric intake and expenditure. Understanding these hormonal pathways provides valuable insights into potential therapeutic targets and interventions for obesity and related metabolic disorders.
ROLE OF LIFESTYLE AND FOOD HABITS IN OBESITY
Lifestyle and food habits play a crucial role in the development and management of obesity. These factors are among the most modifiable elements affecting an individual’s risk of becoming obese.
Consuming foods high in calories but low in nutrients, such as fast foods, sugary snacks, and beverages, contributes significantly to weight gain. These foods can lead to an energy surplus, which the body stores as fat. Increased portion sizes in restaurants and packaged foods encourage overeating, making it easy to consume more calories than needed. Frequent snacking, eating out of boredom, or emotional eating can lead to excessive calorie consumption.
Diets high in processed foods are often rich in added sugars, fats, and salt, while being low in essential nutrients, fiber, and antioxidants. This imbalance can promote weight gain and affect metabolic health. Low intake of fiber, found in whole fruits, vegetables, and whole grains, can affect satiety and gut health, contributing to obesity. Diets unbalanced in macronutrients (carbohydrates, fats, and proteins) can impact metabolic health. For example, excessive intake of refined carbohydrates and unhealthy fats may promote insulin resistance and fat accumulation.
A sedentary lifestyle, characterized by prolonged periods of inactivity and minimal physical exercise, decreases the number of calories burned and contributes to weight gain. Regular physical activity is crucial for maintaining a healthy weight, improving muscle mass, and boosting metabolic health. A lack of exercise can lead to obesity over time.
Inadequate or poor-quality sleep can disrupt hormonal balances that regulate hunger and appetite, specifically increasing levels of ghrelin (hunger hormone) and decreasing levels of leptin (satiety hormone), leading to increased food intake and weight gain.
Chronic stress can lead to an increase in the hormone cortisol, which has been linked to increased abdominal fat. Stress can also lead to emotional eating and choosing high-calorie comfort foods.
High alcohol intake can contribute to weight gain due to its high caloric content and the tendency to eat more when drinking. Eating habits and activity levels are often influenced by family, friends, and social contexts. Unhealthy habits can be contagious within social networks. Easy access to inexpensive, high-calorie foods and limited access to affordable, healthier food options can promote unhealthy eating habits.
Lifestyle and food habits significantly impact the risk of developing obesity. Addressing these factors through individual behavioral changes, as well as public health initiatives aimed at creating healthier food environments and encouraging physical activity, is essential for preventing and managing obesity. Making informed choices about diet, ensuring regular physical activity, managing stress, and getting enough sleep are key strategies for maintaining a healthy weight and improving overall health.
MIT APPROACH TO THE TREATMENT OF OBESITY
Appetite-increasing drugs, also known as orexigenic agents, are used to stimulate appetite in individuals who may be experiencing unintentional weight loss, muscle wasting, or a lack of appetite due to various medical conditions. Examples are Megestrol Acetate, Dronabinol, Oxandrolone, Prednisone, Cyproheptadine, Mirtazapine etc. According to MIT perspective, molecular imprints of these drugs in 30c could be used for reducing appetite and obesity. Drugs potentized above 12c will not contain any drug molecules, but their molecular imprints only. As such, they cannot produce any harmful effects.
Based on the study of pathophysiology of obesity discussed above, according to MIT understanding, Insulin 30, Leptin 30, Ghrelin 30, Cortisol 30, Testosterone 30, Estrogen 30, Thyroidinum 30, Metformin 30 etc should be the main drugs in the therapeutics of obesity.
MIT or Molecular Imprints Therapeutics refers to a scientific hypothesis that proposes a rational model for biological mechanism of homeopathic therapeutics.
According to MIT hypothesis, potentization involves a process of ‘molecular imprinting’, where in the conformational details of individual drug molecules are ‘imprinted or engraved as hydrogen- bonded three dimensional nano-cavities into a supra-molecular matrix of water and ethyl alcohol, through a process of molecular level ‘host-guest’ interactions. These ‘molecular imprints’ are the active principles of post-avogadro dilutions used as homeopathic drugs. Due to ‘conformational affinity’, molecular imprints can act as ‘artificial key holes or ligand binds’ for the specific drug molecules used for imprinting, and for all pathogenic molecules having functional groups ‘similar’ to those drug molecules. When used as therapeutic agents, molecular imprints selectively bind to the pathogenic molecules having conformational affinity and deactivate them, thereby relieving the biological molecules from the inhibitions or blocks caused by pathogenic molecules.
According to MIT hypothesis, this is the biological mechanism of high dilution therapeutics involved in homeopathic cure. According to MIT hypothesis, ‘Similia Similibus Curentur’ means, diseases expressed through a particular group of symptoms could be cured by ‘molecular imprints’ forms of drug substances, which in ‘molecular’ or crude forms could produce ‘similar’ groups of symptoms in healthy individuals. ‘Similarity’ of drug symptoms and diseaes indicates ‘similarity’ of pathological molecular inhibitions caused by drug molecules and pathogenic molecules, which in turn indicates conformational ‘similarity’ of functional groups of drug molecules and pathogenic molecules. Since molecular imprints of ‘similar’ molecules can bind to ‘similar ligand molecules by conformational affinity, they can act as the therapeutics agents when applied as indicated by ‘similarity of symptoms. Nobody in the whole history could so far propose a hypothesis about homeopathy as scientific, rational and perfect as MIT explaining the molecular process involed in potentization, and the biological mechanism involved in ‘similiasimilibus- curentur, in a way fitting well to modern scientific knowledge system.
If symptoms expressed in a particular disease condition as well as symptoms produced in a healthy individual by a particular drug substance were similar, it means the disease-causing molecules and the drug molecules could bind to same biological targets and produce similar molecular errors, which in turn means both of them have similar functional groups or molecular conformations. This phenomenon of competitive relationship between similar chemical molecules in binding to similar biological targets scientifically explains the fundamental homeopathic principle Similia Similibus Curentur.
Practically, MIT or Molecular Imprints Therapeutics is all about identifying the specific target-ligand ‘key-lock’ mechanism involved in the molecular pathology of the particular disease, procuring the samples of concerned ligand molecules or molecules that can mimic as the ligands by conformational similarity, preparing their molecular imprints through a process of homeopathic potentization upto 30c potency, and using that preparation as therapeutic agent.
Since individual molecular imprints contained in drugs potentized above avogadro limit cannot interact each other or interfere in the normal interactions between biological molecules and their natural ligands, and since they can act only as artificial binding sites for specific pathogentic molecules having conformational affinity, there cannot by any adverse effects or reduction in medicinal effects even if we mix two or more potentized drugs together, or prescribe them simultaneously- they will work.
REDEFINING HOMEOPATHY 