Obesity: A National Metabolic Emergency

Obesity is one of the most misunderstood—and deliberately oversimplified—conditions in modern medicine. It isn’t simply the mechanical accumulation of calories; it is the full-body symptom of a breakdown in metabolic communication between hormones, minerals, mitochondria, and the brain’s energy-sensing centers. When that communication collapses, weight becomes just the visible side of a much deeper biochemical crisis. Obesity and type 2 diabetes epidemics have joined forces, ravaging the health of hundreds of millions of people around the world.

Obesity is most often a manifestation of a deeper metabolic disorder. Just labeling it a “disease” allows pharmaceutical companies to prescribe more drugs and insurance systems to bill more codes—but it obscures the chain of cause and effect. However, Obesity (typically defined as BMI ≥30 kg/m²) profoundly impacts metabolic health and elevates cardiovascular disease (CVD) risk through mechanisms like chronic inflammation, insulin resistance, dyslipidemia, hypertension, and endothelial dysfunction. Excess adipose tissue, particularly visceral fat (around organs), releases pro-inflammatory cytokines and free fatty acids, promoting atherosclerosis, heart failure, and type 2 diabetes.

Is it possible to be obese and healthy? The concept of metabolically healthy obesity (MHO) describes obese individuals without traditional metabolic abnormalities (e.g., normal blood pressure, lipids, glucose, and no insulin resistance). Prevalence varies, but long-term data indicate MHO is often transient—30–50% transition to metabolically unhealthy obesity over 4–20 years due to aging, weight gain, or adipose dysfunction.

Thus, obesity is a primary factor related to type 2 diabetes, hypertension, arthritis, gout, and menstrual abnormalities. It has also been linked to several other types of diseases, such as atherosclerosis, cardiovascular disease, adverse effects in the lipid profile of the blood, sleep apnea, osteoarthritis, complications in pregnancy and surgery, some cancers, and gallbladder disease. The deposition of body fat in the abdominal area is more strongly related to disease than the deposition of fat in the peripheral portion (legs).

New Definition of Obesity Means 75% of Americans are Obese

A new definition of obesity is nearly doubling the prevalence of U.S. adults with the condition. For decades, doctors have relied on body mass index (BMI) — a tool that uses height and weight to estimate body fat — to determine obesity. Now, medical scientists are redefining obesity by adding body fat and health status to BMI. A team of researchers from Beth Israel Deaconess Medical Center, Harvard University, Yale University, and Yale New Haven Health found that BMI alone may significantly underestimate the number of U.S. adults with obesity.

Using the new definition that includes waist-based measurements, the team found that more than 75% of adults may meet criteria for obesity compared to 40% when using BMI alone. As of the most recent national data, the majority of American adults—well over half—now meet criteria for some degree of metabolic dysfunction, and if you include pre‑diabetes and early insulin‑resistance, the figure edges toward 70 to 80 percent.

Roughly three of every four American adults now exhibit laboratory or clinical evidence of metabolic dysregulation — ranging from mild insulin resistance to full type 2 diabetes. That makes metabolic syndrome not a niche condition but the defining chronic disorder of modern civilization. It is the soil from which cardiovascular disease, fatty‑liver disease, dementia, and most cancers now grow.

Obesity is a visible symptom of invisible metabolic chaos—nutritional, hormonal, and environmental. Treating it as a primary disease encourages pharmaceutical dependence rather than systemic healing. If 75 percent of Americans now qualify as obese by the new criteria, that number describes a national metabolic emergency, not a new diagnostic insight.

What Actually Causes Obesity

There is not one cause—there are many overlapping drivers that all damage the same regulating pathway: cellular metabolism.

All these converge on one outcome: the body becomes insulin‑resistant, mitochondria shift to low‑oxygen fermentation, cellular pH drops, and fat storage becomes the safest place for toxic and unburnable energy substrates.

Obesity: The New Gold Mine for Pharmaceutical Companies

But redefining the term doesn’t solve the underlying physiology:

• It medicalizes nearly the entire population.
• It distracts from the deeper issues—industrial food, mineral-deficient soil, 24-hour stress culture, and pharmaceutical endocrine disruption.
• It risks pushing costly weight‑loss drugs (GLP-1 agonists) as a mass solution, locking people into another chronic‑management model without metabolic repair.

In other words, the reclassification describes reality—because the metabolic collapse is real—but it also conveniently expands a market for money-hungry pharmaceutical companies.

Instead of “fighting fat,” medicine must address the terrain that produces it:

1. Restore insulin and magnesium balance.
2. Rebuild mitochondrial efficiency through oxygenation and movement.
3. Neutralize chronic acidity via bicarbonate buffering and mineral saturation.
4. Heal circadian rhythm and stress chemistry.
5. Detoxify obesogenic pollutants.

Ozempic and Wegovy: Dangerous Drugs Good For Everything

Many people who successfully lost weight on Ozempic and other GLP-1 agonist drugs are having trouble weaning themselves off the injectables, according to the BBC, because the hunger for food comes roaring back with a vengeance — and hence the pounds start creeping up again, hinting that patients are likely to develop life-long dependencies on the substances. Meaning GLP-1 drugs are as addictive as heroin. Novo Nordisk stock closed flat after a report that its oral Wegovy pill clocked 18,000 prescriptions in its second week.

Ozempic (semaglutide) is a GLP-1 receptor agonist used mainly for type 2 diabetes and increasingly for weight loss (off-label or via Wegovy). Like all GLP-1 drugs, it has a very predictable side-effect profile because of how it slows stomach emptying, alters appetite, and affects the pancreas. Now, with the advent of oral pills of GLP-1, it will be easier and cheaper to get addicted. Many, if not all, who use GLP-1 drugs are going to be exposed to some or many of its dangers.

Summary of Side Effects and Dangers

GLP-1 drugs such as Ozempic, Wegovy, and oral semaglutide work by slowing gastric emptying, suppressing appetite, and altering insulin signaling, which creates a predictable profile of gastrointestinal side effects, including nausea, vomiting, constipation, diarrhea, bloating, and abdominal pain. More serious but less common risks include pancreatitis, gallbladder disease, kidney injury from dehydration, worsening of diabetic retinopathy, and thyroid C-cell tumor signals.

Because these drugs drive rapid caloric reduction, they often cause loss of lean muscle mass and bone density, with a high likelihood of weight and metabolic rebound once treatment stops. For some individuals with underlying conditions—particularly gallbladder disease, pancreatitis, or MEN-2—use is contraindicated, and long-term safety data for young and otherwise healthy users remains limited.

How This Approach Misses the Root Causes of Obesity

Using GLP-1 agonists for weight loss addresses symptoms rather than the biological terrain that produces obesity in the first place. Obesity is fundamentally driven by metabolic dysfunction—insulin resistance, disrupted mitochondrial energy production, hormonal imbalances, circadian misalignment, toxins, ultra-processed diets, sodas, chronic stress, sleep deprivation, and nutrient deficiencies—not by a deficiency of GLP-1 activity.

When a drug forcibly reduces appetite without restoring metabolic health, muscle strength, thyroid function, micronutrient status, or mitochondrial capacity, the body remains in the same dysfunctional state, only with fewer calories. This is why weight often returns when the drug is stopped, and why patients can end up metabolically weaker than before. In this sense, GLP-1 drugs function like appetite silencers rather than true metabolic therapies—and for a population that is structurally overfed but undernourished, this is the wrong tool for the wrong problem. However, the drugs are selling like hotcakes.

Obesity and Cancer

Overweight or obese people are more prone to getting cancer, and yet have cancer blamed on genes instead of real causes like nutritional deficiencies, toxicity, low oxygen, carbon dioxide levels, etc. Obesity is positively associated with an increased risk of breast and prostate cancer and other forms of cancer.

Obesity drives cancer progression and is estimated to account for 14% of all cancer deaths in men and 20% in women in the United States. In comparison, approximately 6% of cancer deaths around the same period of time in Europe were attributed to obesity. According to a report on the global cancer burden, published in 2014, obesity is responsible for an estimated 500,000 cancer cases worldwide each year.

Obesity and Malnutrition

One would think that eating too much would provide cells with an abundance of nutrients. However, being overweight and undernourished is a reality that is just now beginning to be understood. It is pretty strange to say to people that the more they eat, the more malnourished they are destined to be.

Overweight people can be suffering from gross malnutrition because the nutritional values of the basic foods we eat have been steadily dropping for the last fifty years, even as toxic exposures increase. Fiber intake also tends to be much lower in obese people, meaning they are eating too many processed white foods with not only the fiber removed but also many of the vitamins and minerals. Some people go as far as saying obesity is starvation.

Obese people generally have hyperinsulinemia (high levels of insulin in the blood), and insulin causes fat to be stored in fat cells. Obese people in general cannot satisfy their body’s demands for energy or nutrients by eating. In this scenario, lethargy, hunger, and stress are not causes of obesity; they are effects of it (due to the internal starvation). Syndrome X, also known as metabolic syndrome, is a combination of insulin resistance, leptin resistance, and glucose intolerance. All of these conditions are precursors to diabetes, heart disease, obesity, and cancer.

Leptin and Magnesium

Magnesium Sits at the Center of Glucose Metabolism.

Leptin is a hormone that signals your brain to feel full. A leptin deficiency can cause overeating, leading to obesity and obesity-related disease. Most people don’t have a leptin deficiency—they have lost leptin sensitivity, called leptin resistance. Much like insulin resistance, it’s possible to have enough leptin, but because your body doesn’t use it effectively, you still feel hungry. Leptin resistance is a serious health issue. Essentially, you are overfeeding your body, but your brain perceives you as starving.

Leptin is produced mainly by white adipose tissue and signals the brain about the body’s energy stores. In a healthy system, rising leptin levels suppress appetite and increase energy use, while low leptin levels have the opposite effect. In diabetes, however, chronically elevated insulin drives leptin levels up, while hypothalamic leptin sensitivity falls; the body shows hyperleptinemia and leptin resistance.

A crucial but still under-recognized component of diabetic mineral dysregulation: the leptin–magnesium axis. It sits at the intersection of endocrinology, metabolism, and renal physiology. High leptin levels appear to be associated with increased urinary magnesium loss. Leptin is a protein of 167 amino acids. The level of circulating leptin is directly proportional to the total amount of fat in the body.

High leptin levels and low magnesium
levels are extremely pro-inflammatory.

“Leptin is the way that your fat stores speak to your brain to let your brain know how much energy is available and, very importantly, what to do with it,” states well-known metabolic specialist and author of the book The Rosedale Diet, Dr. Ron Rosedale.

When leptin is working correctly, it prevents nutrient spillover by telling insulin to shut off after your tank is full. Every time you eat food in excess (of energy required by the body), leptin and insulin levels surge. Leptin resistance leads to insulin resistance, which in turn perpetuates leptin resistance.

Researchers have found that a proper diet and regular exercise have the most significant effect on reversing the damage caused by leptin resistance. Low-carbohydrate, high-protein diets are beneficial, as are diets that include good fats. This can facilitate weight loss and help to fight leptin resistance.

The body requires magnesium to absorb and utilize nutrients. Without magnesium, the body cannot correctly use the fats, proteins, and carbohydrates we eat every day. When we aren’t getting what we need from our diet, the body will crave more food to obtain those vital nutrients. By activating hundreds of enzymes in the body, magnesium helps you get the most from what you eat, so your body can be satisfied with the amount of food you genuinely need.

Conditions like insulin resistance and diabetes are strongly associated with magnesium deficiency and obesity. Controlling blood sugar levels is a key factor in maintaining a healthy weight. When enough magnesium is present in the body, insulin can function properly, and blood glucose is more easily used for energy. A magnesium deficiency impairs insulin function, leading to high blood sugar and increased fat storage.

Leptin and magnesium both act as endocrine regulators. Leptin functions primarily as the body’s energy‑inventory signal:

• Secreted by fat cells.
• Tells the hypothalamus how much energy is stored.
• Suppresses appetite, increases thermogenesis, and modulates insulin sensitivity.

Both leptin excess and Mg deficiency aggravate anxiety, fatigue, and abnormal pain perception—all common in diabetic neuropathy. In diabetes or insulin resistance, leptin levels often rise abnormally (hyperleptinemia). Yet the brain and tissues become insensitive to it (leptin resistance).

High circulating leptin also acts on the kidneys, increasing sodium excretion (natriuresis) and water output (diuresis). This renal action was originally protective—preventing salt retention in obesity—but in diabetes, it causes collateral mineral loss, particularly magnesium through the distal convoluted tubule. High leptin → more renal Mg wasting. That loop gradually creates a hypomagnesemic, hyperleptinemic spiral.

Understanding and correcting this loop is one of the subtle frontiers of endocrinology: the point where mineral balance and hormonal control merge into a single metabolic conversation.

Improving magnesium intake—by diet (green vegetables, nuts, seeds, mineral-rich water) or appropriate supplementation—often lowers circulating leptin, enhances insulin sensitivity, and reduces inflammatory markers. It also helps blunt the diuretic magnesium loss driven by leptin. Because leptin secretion itself follows circadian and thyroid cues, restoring sleep rhythm, thyroid adequacy, and general metabolic balance reinforces magnesium’s benefit.

In short, high leptin and low magnesium are two sides of the same metabolic coin. Correcting magnesium deficiency doesn’t just replace a mineral; it rebalances the entire hormonal conversation among fat tissue, kidneys, pancreas, and brain.

Eating throws powerful hormonal switches, and it’s just as important when you eat as what you eat, states Byron Richards, leptin expert of Wellness Resources. He provides 5 simple rules for getting the leptin in our systems to work properly for you and help you lose weight:

I do not totally agree with Richards; two meals a day leaves room for intermittent fasting, which provides time for autophagy, allowing cells to be detoxified. Autophagy is the cellular “self-cleaning” or detoxification process that ramps up during periods without food — such as in the morning before eating, during fasting, or overnight. It literally means “self-eating” from Greek, referring to the recycling of damaged proteins, toxins, and dysfunctional mitochondria.

Further Complications of GLP-1

GLP-1 agonists (like Ozempic, Wegovy, oral semaglutide) slow gastric emptying and frequently cause gastrointestinal side effects, especially during dose escalation:

• Nausea
• Vomiting
• Diarrhea
• Poor appetite

These GI effects can lead to:

• Reduced food intake
• Reduced intake of magnesium-rich foods
• Impaired absorption
• Increased loss through diarrhea

If these persist, total body magnesium stores can fall over time because:

• dietary intake is low,
• losses in stool are high,
• and GI transit time is altered.

Weight Loss Itself Can Affect Magnesium

Rapid weight loss—especially when calories are dramatically reduced—can alter:

• intracellular magnesium distribution
• the balance between muscle/organ stores and circulating levels
• Magnesium is used in metabolic adaptation.

In other words, net magnesium demand may rise, and yet dietary intake may not keep up,

• Blood levels can fall even if intestinal absorption is normal.

Thus, weight loss, not the GLP-1 molecule itself, often plays a significant role in worsening magnesium deficiencies that are already deteriorating over time.