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Just steve's avatar
Just steve
10h

The most troubling part of this article is knowing more than one person, non-drinkers although overweight having very likely died from this. More negatives from Ultra Processed Foods and also likely toxic overload for all us trying to swim through the toxic sea so many of the general public, despite being very active for over half a century attempting to clean our environment up.

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Guillermou's avatar
Guillermou
15h

We must remember that fatty liver can often lead to fibrosis. Dr. Mercola also reported that in the U.S., an estimated 30% of adults have non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease. In people with obesity, up to 90% have NAFLD, as do up to 75% of those who are overweight, 50% of people with diabetes, and even 10% of American children. Ultra-processed foods loaded with fructose and trans fats, increased intake of industrially processed, toxic seed oils, and environmental pollutants such as glyphosate and PFAS are risk factors.

Liver ultrasound, also known as sonography, is a diagnostic procedure that uses high-frequency sound waves to create images of the liver and other abdominal organs. The test is non-invasive, meaning no incisions or injections are needed, and is considered one of the safest imaging techniques available.

Liver ultrasound is a non-invasive imaging test that uses sound waves to create images of the liver and its surrounding structures. It is one of the most common diagnostic tools used to assess liver health, detect abnormalities, and monitor liver conditions. This test plays a crucial role in diagnosing a variety of liver-related diseases, including fatty liver disease, cirrhosis, hepatitis, and liver tumors.

https://www.apollohospitals.com/es/diagnostics-investigations/liver-ultrasound .-- https://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S2529-850X2020000400004.--- Liver elastography is currently one of the key tools for evaluating liver fibrosis without the need for a biopsy. It measures the "stiffness" of liver tissue, which increases when fibrosis or cirrhosis is present. It is an ultrasound (or MRI)-based technique that quantifies liver stiffness in kilopascals (kPa). The most commonly used: It is an ultrasound (or MRI)-based technique that quantifies liver stiffness in kilopascals (kPa). The most commonly used techniques:

1) Transient elastography (FibroScan) → the most widespread

2) Ultrasound elastography (ARFI, SWE)

3) Magnetic resonance elastography (more accurate, more expensive)

4) Main clinical applications

5) Fatty liver disease (NAFLD/MASLD)

6) Hepatitis B and C

7) Alcoholic liver disease

8) Monitoring fibrosis progression or regression

9) Determining the need for biopsy or treatment

https://www.aasld.org/practice-guidelines?utm_source=chatgpt.com

https://pubmed.ncbi.nlm.nih.gov/?term=liver+elastography+fibrosis&utm_source=chatgpt.com

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-tumor microenvironment, connecting molecular insights with clinical outcomes.

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

Several factors can cause or contribute to the development of fatty liver disease, including:

1) Obesity.

2) Excess abdominal fat (people of normal weight can develop fatty liver disease if they have “visceral obesity,” meaning they have a lot of fat around their waist).

3) Insulin resistance.

4) High intake of refined carbohydrates.

5) Consumption of sugary drinks.

6) Impaired gut health.

Any of these situations will cause your liver to begin accumulating fat between its cells, inflaming them. This is what we know as non-alcoholic fatty liver disease. Among the consequences of having fatty liver disease are developing fibrosis, cirrhosis, and even liver cancer. In some cases, the health situation becomes so complicated that the only treatment option is a liver transplant.

PRINCIPLES OF NUTRITION IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE

https://www.intechopen.com/online-first/1199119 .---

ADVANCEMENTS IN UTILIZING NATURAL COMPOUNDS FOR MODULATING AUTOPHAGY IN LIVER CANCER: MOLECULAR MECHANISMS AND THERAPEUTIC TARGETS

https://www.mdpi.com/2073-4409/13/14/1186 .---

THERAPEUTIC EFFECTS OF NATURAL PRODUCTS ON LIVER CANCER AND THEIR POTENTIAL MECHANISMS

https://www.mdpi.com/2072-6643/16/11/1642.---

NATURAL PRODUCTS AS HEPATOPROTECTIVE AGENTS—A COMPREHENSIVE REVIEW OF CLINICAL TRIALS

https://pmc.ncbi.nlm.nih.gov/articles/PMC11280762/ .-

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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