Calculating TDEE

Identifying hormonal imbalances (signs and symptoms)

Introduction: From Vague Symptoms to Actionable SignaturesWe will now move beyond isolated complaints like "fatigue" or "weight gain." Instead, this section teaches how to identify "symptom signatures"—distinct clusters of signs and patterns of physical change that point directly to an underlying hormonal driver.

This is the art of listening to your body's biochemistry.

Your body doesn't speak in words; it speaks in symptoms, and this section is your translation guide. Part I: The Signatures of Core Metabolic DysfunctionThis part revisits the "big three" hormones from earlier sections, but shifts the focus from their internal mechanisms to their external manifestations.1. The Insulin Resistance Signature: Reading the Warnings on Your Skin and WaistlineIn its early stages, insulin resistance is a silent condition. The body compensates for the cells' deafness to insulin by forcing the pancreas to produce more of it (hyperinsulinemia), a strategy that successfully keeps blood sugar in a normal range while the underlying problem worsens.^[1] The first tangible signs are often subtle and easily dismissed, but they are critical warnings. The "Canary in the Coal Mine": Acanthosis Nigricans (AN)One of the most powerful and specific early warning signs of severe insulin resistance is a skin condition called acanthosis nigricans (AN). It appears as dark, velvety, thickened patches of skin, typically in body folds like the back of the neck, armpits, and groin.^[1] These patches can sometimes be itchy or develop an odor.^[5] This is not a simple cosmetic issue; it is a direct, external manifestation of a severe internal hormonal state. The extreme levels of insulin circulating in the blood "spill over" and begin to bind with high affinity to receptors for a related hormone, Insulin-like Growth Factor 1 (IGF-1), which are abundant on skin cells called keratinocytes and fibroblasts.^[6] This cross-reaction triggers a cascade of rapid, abnormal cell proliferation, leading to the characteristic thickened and pigmented appearance.^[9] In essence, AN is a non-invasive biomarker, making an invisible internal process visible on the skin's surface. Its presence is a strong predictor of future diabetes, and its severity can even correlate with fasting insulin levels.^[5] The appearance of AN, or its common companion, skin tags, is an urgent signal to investigate metabolic health, even if blood glucose tests are still "normal".^[1] The Metabolic Syndrome Scorecard: Quantifying Your RiskMetabolic Syndrome is not a single disease but a cluster of conditions that, when present together, dramatically increase the risk of cardiovascular disease, stroke, and type 2 diabetes. It is, at its core, a clinical proxy for significant insulin resistance. The criteria defined by the National Institutes of Health (NIH) and the American Heart Association (AHA) serve as a powerful, evidence-based scorecard for self-assessment. The presence of three or more of the following five criteria indicates a state of advanced metabolic dysfunction.^[11] Central Obesity: Waist circumference greater than 40 inches (102 cm) for men or 35 inches (89 cm) for women. This measurement is critical because it reflects an accumulation of visceral fat, the metabolically active fat surrounding the organs that releases inflammatory cytokines and directly worsens insulin resistance.^[14] High Triglycerides: A fasting level of 150 mg/dL or higher. This indicates that the liver, faced with excess glucose that cells can no longer accept, is working overtime to convert that sugar into fat for storage.^[2] Low HDL ("Good") Cholesterol: Less than 40 mg/dL for men or 50 mg/dL for women.

This is a key feature of the atherogenic dyslipidemia characteristic of insulin resistance, signaling an unhealthy pattern of cholesterol transport.^[13] High Blood Pressure: A reading of 130/85 mmHg or higher, or being on medication for hypertension. Chronic hyperinsulinemia can contribute to high blood pressure by affecting kidney function and the flexibility of blood vessels.^[14] High Fasting Blood Sugar: A level of 100 mg/dL or higher.

This is often the last of the five criteria to appear, as it signifies that the pancreas is finally beginning to fail in its ability to produce enough insulin to overcome the profound resistance in the body's cells.^[1] The Experiential ClusterThese clinical signs are accompanied by a distinct set of daily experiences. These can include reactive hypoglycemia—energy crashes, irritability, and intense cravings for carbohydrates that occur one to three hours after a high-carb meal—as well as a persistent, gnawing hunger even after eating (polyphagia).^[3] As the condition progresses toward prediabetes, increased thirst and frequent urination become more common as the body attempts to flush out excess glucose.12. The Cortisol Overload Signature: The Physical Manifestations of Chronic StressChronic stress manifests in a unique pattern of physical changes driven by the persistent elevation of cortisol. The Body Shape Transformation: Central Adiposity and Muscle WastingCortisol is not merely a fat-storage hormone; it is a fat-redistributing hormone. It actively mobilizes fat from the extremities (arms and legs) and preferentially deposits it as deep visceral fat within the abdomen, leading to the characteristic "cortisol belly".^[18] This redistribution can also appear as fat pads on the upper back (a "buffalo hump") and a rounding of the face ("moon face").^[20] This accumulation of central fat is starkly contrasted by cortisol's catabolic (breakdown) effect on protein. To supply the liver with raw materials for glucose production (gluconeogenesis), chronically high cortisol breaks down muscle tissue in the arms and legs. This results in a characteristic body shape: a thick, heavy trunk with thinning limbs.^[20] This muscle wasting is also the source of symptoms like progressive muscle weakness and difficulty rising from a seated position.^[23] Skin Integrity CollapseCortisol's protein-destroying effects extend to the collagen that provides structure and resilience to the skin. This leads to thin, fragile skin that bruises easily.^[20] When this weakened skin is stretched by the rapid accumulation of abdominal fat, it tears, resulting in the formation of wide, purplish stretch marks known as striae.^[20] The HPA-HPG Axis CollisionChronic stress is a state of sustained Hypothalamic-Pituitary-Adrenal (HPA) axis activation.

This creates a direct physiological conflict with the Hypothalamic-Pituitary-Gonadal (HPG) axis, which governs reproduction and anabolic (building) processes. From an evolutionary perspective, the body, perceiving a constant threat to survival, logically prioritizes the "fight or flight" response over non-essential functions like reproduction.^[25] High levels of cortisol directly inhibit testosterone production and disrupt the delicate hormonal cascade that regulates the menstrual cycle.^[20] Therefore, symptoms like low libido, erectile dysfunction in men, or irregular and absent periods in women are not separate issues from their stress and weight gain; they are part of the same symptom signature of HPA axis dominance.^[30] The Neuro-Behavioral ClusterThese physical signs are invariably linked to a psychological experience of being "wired but tired." This includes anxiety, irritability, restlessness, and disrupted sleep, especially waking in the middle of the night with a racing mind.^[22] This state is often accompanied by intense cravings for high-fat, high-sugar "comfort foods," which provide a temporary neurochemical reward that briefly dampens the stress response.183. The Leptin Resistance Signature: The Paradox of Insatiable HungerUnlike insulin or cortisol, leptin resistance has few unique physical signs. Its signature is primarily behavioral and experiential, defined by a profound dysregulation of hunger and satiety. Behavior as the Primary SymptomThe cardinal symptom is hyperphagia: an intense, insatiable hunger that is not relieved by eating a meal.^[17] The brain's hypothalamus, which should be receiving leptin's "we have enough energy" signal, is functionally blind to the body's ample fat stores. Instead, it is screaming "starvation," compelling the individual to eat more.^[32] This manifests as the feeling of a broken "off switch," an inability to stop eating once started, constant thoughts of food, and powerful, seemingly uncontrollable cravings.^[34] This is not a failure of willpower; it is a biological signal gone haywire. The Biology of the "Yo-Yo" DietLeptin resistance provides the biological explanation for the frustrating cycle of weight loss and regain. When a person with this condition successfully loses weight through calorie restriction, their fat mass decreases. This causes a significant drop in their circulating leptin levels.^[32] The already-resistant brain interprets this sharp drop in the leptin signal not as a successful outcome, but as a catastrophic famine. In response, it triggers a powerful, evolutionarily conserved "starvation response": metabolic rate plummets to conserve energy, while hunger and cravings skyrocket to force the body to regain the lost weight and "survive" the perceived famine.^[32] This reframes the common experience of weight regain from a personal failure to a predictable hormonal consequence that requires a strategy far more nuanced than simple calorie restriction. Part II: Key Co-Conspirators and Overlapping SyndromesThe "big three" do not operate in a vacuum. Their dysfunction is often intertwined with other hormonal systems.4. The Thyroid Slowdown: When the Metabolic Engine CoolsAn underactive thyroid (hypothyroidism) slows the body's entire metabolic rate. While symptoms like fatigue and weight gain overlap with other imbalances, the hypothyroid signature has several key differentiators. The classic checklist includes pervasive fatigue and lethargy, an unusual intolerance to cold (feeling cold when others are comfortable), modest but stubborn weight gain, constipation, dry skin, and hair loss—which can uniquely include the outer third of the eyebrows.^[37] The combination of cold intolerance, constipation, and these characteristic skin and hair changes is highly suggestive of a primary thyroid issue.5. Sex Hormone Imbalances: Drivers of Body Composition, Mood, and MoreLow Testosterone (Men and Women)Testosterone is a primary anabolic hormone in both sexes. Its deficiency signature is one of declining drive and structure: decreased muscle mass, increased body fat (especially visceral fat), low motivation, fatigue, low libido, and cognitive issues often described as "brain fog".^[41] In men, this can become a self-perpetuating vicious cycle driven by the enzyme aromatase, which is highly active in fat tissue and converts testosterone into estrogen.^[45] As a man gains excess body fat, particularly in the context of insulin resistance which further stimulates aromatase, more of his testosterone is converted into estrogen.^[45] This leads to falling testosterone levels (causing more muscle loss and fat gain) and rising estrogen levels (which can cause gynecomastia and worsen metabolic health), creating a hormonal environment that accelerates the very problem that started it.^[47] Estrogen Dominance (Primarily Women)Estrogen dominance is defined by a high estrogen-to-progesterone ratio. Its signature is often cyclical, tied to the menstrual cycle. Key signs include severe premenstrual syndrome (PMS) with mood swings, bloating, and breast tenderness; heavy, painful, or irregular periods; the development of uterine fibroids; and a characteristic pattern of fat storage on the hips and thighs.^[48] A key contributor to this state can be found in the gut. The "estrobolome" is the collection of gut bacteria capable of metabolizing estrogens.^[52] The liver packages up excess estrogen for disposal through the gut.

However, an unhealthy gut microbiome (dysbiosis) can have an overgrowth of bacteria that produce an enzyme called beta-glucuronidase.^[52] This enzyme effectively "unpackages" the estrogen in the gut, allowing it to be reabsorbed back into circulation instead of being eliminated. This process increases the body's total estrogen load, providing a direct mechanistic link between gut health and systemic hormonal imbalance. Part III: Synthesis and Action: Your Personal Hormonal AuditThe following table is designed to help you move from a list of symptoms to a recognizable pattern. It is not a tool for self-diagnosis but for strategic prioritization. While symptoms often overlap, the dominant pattern is the key to identifying where to focus your efforts using the four pillars outlined in Section 4.