Diet and nutritionHormones and weight gain — is it not gluttony, but hormone balance?
- Andrzej Frydrychowski — Menopauza - jak nie oszaleć i pozostać kobietą?
- Bracia Rodzeń — Bracia Rodzeń
- Henryk Różański — Choroba Hashimoto, czyli przewlekłe autoimmunologiczne zapalenie tarczycy, część 1.
- Henryk Różański — Powstawanie Cellulitis – cellulit
- Thomas E. Levy — Dr. Thomas Levy
- Nathan S. Bryan — The Energy of Life - How Do We Capture & Optimize Our Energy Output?
- Hormonal changes in PCOS. · J Endocrinol 2024
- Hormones and obesity. · Baillieres Clin Endocrinol Metab 1994
- The hypothalamus, hormones, and hunger: alterations in human obesity and illness. · Prog Brain Res 2006
- Obesity and endocrine disease. · Endocrinol Metab Clin North Am 2003
- [Leptin]. · Rev Invest Clin 2002
- Incretin hormones, obesity and gut microbiota. · Peptides 2024
- Impact of Sleeve Gastrectomy on Obesity Indices, Reproductive Hormones, and Ovarian Reserve Markers: A 12-Month Prospective Study. · Obes Surg 2026
- Impact of Bariatric Surgery on Reproductive Hormones and Menstrual Regularity in Women with Obesity. · Obes Surg 2026
- Orthomolecular Medicine News Service — Understanding and Addressing Vitamin D Resistance: A Comprehensive Approach Integrating Genetic, Environmental, and Nutritional Factors
- Orthomolecular Medicine News Service — The ICV Axis: A Practical, Clinically Actionable Breakthrough for BHRT and Metabolic Medicine
- Orthomolecular Medicine News Service — Vitamin C and Cortisol: Synergistic Infection and Toxin Defense
Nathan S. Bryan links weight gain to dysfunction in cells of the digestive system, and hormone disorders to insufficient energy production in cells of the endocrine system.
- Andrzej Frydrychowski points out that during menopause, a slower metabolism may accompany weight gain, while mood swings can encourage snacking.
- Henryk Różański describes the effect of thyroid hormones on basal metabolic rate and links estrogen to cellulite and progesterone to water retention in tissues.
- The Rodzeń brothers link higher carbohydrate intake to weight gain, while Thomas E. Levy attributes fat gain to sugars and carbohydrates and links insulin spikes to increased hunger and overeating.
What the authors write
During menopause, a slower metabolism may accompany weight gain, while mood swings can encourage snacking.
After eating carbohydrates, insulin levels rise and signal the body to store energy; the Rodzeń brothers link higher carbohydrate intake to weight gain.
Thyroid hormones stimulate basal metabolic rate.
Estrogen is linked to the development of cellulite, while progesterone is linked to water retention in connective and fatty tissue.
Thomas E. Levy attributes fat gain to sugars and carbohydrates, not dietary fat.
Thomas E. Levy links insulin spikes after eating carbohydrates to increased hunger and overeating.
Nathan S. Bryan links dysfunction in cells of the digestive system to weight gain, and insufficient energy production in cells of the endocrine system to hormone disorders.
Research from PubMed · Europe PMC
We selected 8 studies with the best, positive results. This is a selection, not a full review of all research.
Total number of studies on this topic in PubMed: 83 801.
The review indicates that hormone disorders in PCOS, including insulin resistance and leptin resistance, are associated with a higher prevalence of obesity.
Aim of the study: Polycystic ovary syndrome (PCOS) is a common endocrinopathy occurring in reproductive-age women. Hyperandrogenism, polycystic ovaries, chronic anovulation, and metabolic aberrations are the common features in PCOS.
Results: These hormones are related to metabolic disorders, such as diabetes and insulin resistance, overweight and obesity, infertility, and disturbed menstrual cycle in PCOS patients. The pathological changes of these hormones, such as increased insulin, reduced GH, increased ghrelin, and leptin resistance, result in an increased prevalence of diabetes and obesity in PCOS women. A reduced GH, increased LEAP-2 levels, high LH basal, increased LH/FSH ratio, high androgens, and low estrogen are demonstrated in PCOS and linked to infertility. This narrative review aims to clarify the changes of hormone profiles, such as insulin, GH, LH, FSH, androgens, estrogen, progesterone, ghrelin, LEAP-2, asprosin, and subfatin, in PCOS, which may reveal novel targets for better diagnosis and treatment of PCOS.
“Not stated” does not mean nobody paid — the database does not always record it.
The review describes hormonal changes associated with obesity and indicates that they may sustain its development.
Aim of the study: This chapter has reviewed the evidence for obesity being characterized by distinct patterns of hormonal changes related to both the degree of obesity and the distribution of fat tissue. Many of these changes are also seen in subjects with Cushing's and polycystic ovary syndromes, in particular hyperinsulinaemia, alterations in adrenocortical activity and sex steroid secretion and binding.
Results: Upper body obesity is characterized by large adipose cells with higher LPL activity, elevated basal and stimulated lipolysis but a low antilipolytic effect of insulin. The results from preliminary investigations of potential candidate genes suggest a possible genetic basis to hyperinsulinaemia/insulin resistance found in upper body obesity but further studies of greater numbers are required for confirmation. It is hoped that the findings from such molecular studies will shed additional light on both the genetic background to obesity and the complex hormonal alterations seen at the tissue level. This should provide the confirmation of a unifying theory for the causal factors associated with obesity and related conditions.
“Not stated” does not mean nobody paid — the database does not always record it.
The review indicates that gut hormone disorders may affect hunger and satiety and encourage obesity.
Aim of the study: Obesity is a major global epidemic, with over 300 million obese people worldwide, and nearly 1 billion overweight adults. Being overweight carries significant health risks, reduced quality of life, and impaired socioeconomic success, with profound consequences for health expenditure.
Results: It remains unproven if their hyperghrelinemia or other gut-hormone abnormalities contribute to the hyperphagia in PWS, in addition to brain defects. Postmortem human hypothalamic studies and generation of animal models of PWS can also provide insight into the pathophysiology of abnormal-feeding behavior. Changes in orexigenic NPY and AGRP hypothalamic neurons, or anorexigenic oxytocin neurons have been found in illness and PWS. Functional neuroimaging studies, using PET and fMRI, will also allow us to tease apart the hormonal and brain pathways responsible for controlling human appetite, and their defects in obesity.
“Not stated” does not mean nobody paid — the database does not always record it.
The review indicates that some hormone disorders may contribute to the development of obesity, although some changes are a consequence of it.
Aim of the study: Several endocrine abnormalities are reported in obesity. Some of these abnormalities are considered as causative factors for the development of obesity, whereas others are considered to be secondary effects of obesity and usually are restored after weight loss.
Results: Also, several endocrine diseases have obesity as one their clinical manifestations. Hypothyroidism, Cushing's syndrome, GH and testosterone deficiency, polycystic ovarian syndrome, insulinoma, hypothalamic lesions, and genetic syndromes often present with obesity. In most of these conditions, appropriate treatment of the primary disease results in weight loss. In addition, the fat cell has been found to be an endocrine organ that produces several peptides that are bioactive and participate in the regulation of adipocyte function.
“Not stated” does not mean nobody paid — the database does not always record it.
The description indicates that leptin is involved in regulating hunger and satiety, and that its level depends, among other things, on hormones and food intake.
Aim of the study: Leptin is a hormone secreted by adipocytes, stomach and placenta. Age, sex, puberty onset and food intake are the most important physiological factors that determines leptin concentration.
Results: Age, sex, puberty onset and food intake are the most important physiological factors that determines leptin concentration. It has been shown that leptin secretion is regulated by other hormones such as insulin, glucocorticoids and sex steroids. Leptin has an important role in hungry and satiety regulation as well as in normal sexual maturation. There have been some studies in obese subjects showing promising results with leptin administration.
“Not stated” does not mean nobody paid — the database does not always record it.
Gut hormones affect appetite and body weight, and the microbiota may regulate their secretion.
Aim of the study: Over the past 40 years, the prevalence of obesity has risen dramatically, reaching epidemic proportions. By 2030 the number of people affected by obesity will reach 1.12 billion worldwide.
Results: The gut microbiota plays an important role in various metabolic conditions, including obesity and type 2 diabetes and influences host metabolism through the interaction with enteroendocrine cells that modulate incretins secretion. Gut microbiota metabolites, such as short-chain fatty acids (SCFAs) and indole, directly stimulate the release of incretins from colonic enteroendocrine cells influencing host satiety and food intake. Moreover, bariatric surgery and incretin-based therapies are associated with increase gut bacterial richness and diversity. Understanding the role of incretins, gut microbiota, and their metabolites in regulating metabolic processes is crucial to develop effective strategies for the management of obesity and its associated comorbidities.
“Not stated” does not mean nobody paid — the database does not always record it.
After bariatric surgery, women’s BMI decreased, and the study also found hormonal changes.
Aim of the study: Severe obesity is associated with hormonal imbalances, hyperandrogenism, and insulin resistance, all of which adversely affect reproductive physiology. Metabolic and bariatric surgery (MBS) produces durable weight loss and metabolic improvement, but its effects on ovarian reserve markers and reproductive hormones in women of reproductive age remain incompletely characterized.
Results: BMI decreased from 42.38 ± 1.41 to 25.65 ± 0.34 kg/m² at 12 months (p < 0.001). AMH declined from 3.13 ± 0.17 to 2.24 ± 0.44 ng/mL; AFC fell from 11.22 ± 1.60 to 7.16 ± 1.63 (right ovary) and from 11.09 ± 1.30 to 6.19 ± 0.86 (left ovary). FSH, LH, and estradiol increased; SHBG nearly doubled (36.26 → 63.77 nmol/L); total testosterone decreased markedly (27.76 → 9.34 ng/dL); FAI fell from 2.73 ± 0.85 to 0.53 ± 0.19; HOMA-IR declined from 3.94 ± 0.46 to 1.66 ± 0.56 (all p < 0.001). Spearman correlations among change scores showed inverse associations between ΔSHBG and ΔFAI (ρ = -0.420, p = 0.017), and between ΔHOMA-IR and Δtotal testosterone (ρ = -0.374, p = 0.035). Sleeve gastrectomy was associated with marked improvements in insulin resistance and androgenic profiles, accompanied by progressive increases in SHBG and reductions in FAI, AMH, and AFC over 12 months.
“Not stated” does not mean nobody paid — the database does not always record it.
After bariatric surgery, body weight decreased, and this weight loss was associated with changes in the levels of some hormones.
Aim of the study: Obesity affects 2.5 billion adults, disrupting the hypothalamic-pituitary-ovarian (HPO) axis through adipokine imbalance and aromatase activity. This causes hormonal dysregulation, infertility, and pregnancy risks. Bariatric surgery can restore hormonal balance and improve menstrual regularity. This study evaluates post-bariatric surgery changes in reproductive hormones and cycle regularity over six months in Egyptian women with obesity.
Results: Bariatric surgery resulted in a highly significant reduction in body weight and BMI over the six-month follow-up period (p < 0.001). Significant hormonal shifts were observed, including increased levels of FSH (p < 0.001) and LH (p = 0.001), a decreased LH/FSH ratio (p = 0.005), and marked reductions in estrogen and progesterone concentrations (p < 0.001). While AMH levels remained stable (p = 0.6), menstrual regularity improved significantly from 20% at baseline to 53.3% post-surgery (p = 0.001). Furthermore, the degree of weight loss was significantly and positively correlated with postoperative FSH and LH levels. The interventions were generally well-tolerated, with 82.4% of participants reporting no postoperative complications. No significant differences in the improvement of weight or hormonal profiles were noted between patients with and without PCOS.
“Not stated” does not mean nobody paid — the database does not always record it.
Perspectives and opinion materials
The content below presents the authors’ opinions, interpretations and hypotheses. It is not treated as equal to scientific studies and systematic reviews.
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