Dr. Mercola's Censored Library (Private Membership)

Dr. Mercola's Censored Library (Private Membership)

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Guillermou's avatar
Guillermou
5dEdited

Dr. Mercola's article highlights the serious risk of insulin resistance and cancer, and we also know the implications of insulin resistance in metabolic diseases in general, such as neurodegenerative and cardiovascular diseases, a true pandemic of the 20th century.

Insulin resistance (IR) is increasingly recognized as a significant factor for cancer development and progression. While the triglyceride-glucose (TyG) index and its derivatives (TyG-BMI (body mass index), TyG-WC (waist circumference), and TyG-WHtR (waist-to-height ratio)) have been developed as reliable and straightforward surrogate tools for reflecting IR status, their comparative associations with pan-cancer incidence and mortality remain unclear. This study aimed to systematically evaluate the associations of these four IR-related indices with pan-cancer incidence and cancer-specific mortality in a large prospective cohort.

IR-related indices, especially TyG-WC, are significantly associated with both pan-cancer incidence and cancer-specific mortality. Compared with TyG, TyG-BMI, and TyG-WHtR, TyG-WC demonstrated stronger associations, suggesting its potential utility for stratifying cancer risk and prognosis in clinical and public health settings.

https://link.springer.com/article/10.1186/s41182-025-00884-5 (2026)-------------------------------

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At the end of 2025, I had a blood test, and my results were: fasting glucose 75, fasting insulin 2.1, and triglycerides 92. An ultrasound and liver elastography revealed a normal liver (no fatty liver or fibrosis).

1. HOMA-IR (insulin resistance)

HOMA-IR = Glucose (mg/dL) × Insulin (μU/mL) / 405 = 75 × 2.1 / 405 = 0.39

Excellent insulin sensitivity

2. QUICKI (inverse index, more sensitive)

QUICKI = 1 / log(Insulin) + log(Glucose) = 1 / log(2.1) + log(75) ≈ 0.46

Excellent sensitivity

3. Glucose/Insulin Index

G/I Index = 75 / 2.1 = 35.7

10 → good sensitivity. 35.7 → exceptional

4. HOMA-β (pancreatic function)

HOMA-β=360×Insulin /Glucose−63= 360 x2.1/ 75 - 63)= 63

Your value: 63 → correct (efficient without hyperinsulinemia)

5. TyG index (indirect hepatic marker)

TyG=ln (Triglycerides ×Glucose / 2= 92x75/2= 8.15 close to optimum

< 8.0 → optimum

8.0–8.5 → intermediate

Greater than 8.5 → risk

CONCLUSION:

Exceptional insulin sensitivity

Very efficient metabolism

Low pancreatic load

Low metabolic and hepatic risk

Hepatic risk: very low

Profile compatible with good mitochondrial function and low inflammation

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This review draws attention to the link between IR and BC, particularly in post-menopausal women. According to the literature, IR, often associated with obesity, T2DM, and inflammatory mediators released from adipose tissue, is linked to both the occurrence and progression of BC. Mechanistic studies provide further evidence that hyperinsulinemia and dysregulated insulin/IGF signaling contribute to BC development by promoting tumor proliferation, survival, and progression. Given that both lifestyle and pharmacological insulin-sensitizing interventions (e.g., structured physical activity or metformin therapy) have evidence supporting improvements in metabolic health and BC outcomes, further study is warranted.

IR is clinically relevant not only for metabolic disorders but also for determining the prevention, prognosis, and treatment of BC. Future studies should help clarify the value of evaluating IR markers such as HOMA-IR and the TyG index to enable early identification of women who may be at high risk for BC and consider tailored prevention and treatment options. Because IR is modifiable through lifestyle and pharmacological interventions, the management of metabolic health in BC has the potential to serve as an inexpensive and practical approach to minimize the risk of recurrence and the morbidity burden among BC survivors. The clinical and research community is urged not only to recognize the metabolic aspect of BC but also to incorporate strategies to improve insulin sensitivity into prevention and overall cancer care. Identifying and targeting IR as a modifiable risk factor creates an avenue to connect metabolic health and oncology to improve patient outcomes.

https://link.springer.com/article/10.1007/s12672-026-04828-1 (2026)----------------------------------------------------------Insulin resistance (IR) is present in most patients with liver disease and is considered a key factor in disease progression.<sup>15</sup> In IR states, peripheral tissues (muscle, adipose tissue) do not respond adequately to insulin, while, paradoxically, hepatic insulin signaling continues to promote lipogenesis through persistent activation of SREBP-1c. This "selective IR" favors triglyceride accumulation in hepatocytes.

In adipose tissue, IR attenuates insulin-mediated suppression of lipolysis, increasing circulating free fatty acids (FFAs). Excess FFAs are transported to the liver, saturating oxidative and export pathways and increasing lipotoxicity. Simultaneously, inflammatory adipokines (leptin, resistin) and infiltrating macrophages reinforce systemic and hepatic inflammation, further impairing insulin signaling. Therefore, insulin resistance (IR) not only promotes lipid accumulation but also establishes a pro-inflammatory and pro-fibrotic environment that accelerates progression to mastitis and fibrosis. Taken together, these IR-driven mechanisms link systemic metabolic dysfunction with organ-specific pathomechanisms in mastitis and liver disease (MASLD). They illustrate how altered insulin signaling contributes not only to lipid accumulation but also to inflammation, oxidative damage, and fibrosis, reinforcing IR as a central orchestrator of MASLD progression, as depicted in Figure 1. The schematic in Figure 2 and Table 2 highlights the interconnected mechanisms linking systemic metabolic dysfunction with hepatocellular carcinoma (HCC). Insulin resistance and lipotoxicity promote chronic inflammation, oxidative stress, and mitochondrial damage, while gut microbiota dysbiosis amplifies immune activation via lipopolysaccharides (LPS) and altered bile acid signaling. Genetic and epigenetic alterations further destabilize genome integrity, facilitating malignant transformation. Unlike tables summarizing individual determinants, this figure provides a visual map of how these processes converge to create a pro-tumoral microenvironment, connecting molecular insights with clinical outcomes.

https://onlinelibrary.wiley.com/doi/full/10.1111/eci.70132 (2026)

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Just steve's avatar
Just steve
5dEdited

Massive industrial farming cranking out commodities untouched by human hands as possible feed Ultra Processed Foods untouched by human hands as possible to deliver massive quantities of empty toxic calories to in turn ramp up Insulin Resistance, gumming up our bodies natural ability to stay in balance, to maintain our health.

For decades it was promoted a calory is just a calory and it didn't matter what we ate and it didn't matter how or when we ate.

Proving to be wrong, so wrong! Just Sayn'

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