Curing a fatty liver...

Anxious1 wrote:abc, i was not being sarcastic i was genuinely interested. can u tell us if u had fatty liver diagnosed by ultrasound, CT scan or MRI, and then had another scan to prove it was cured?

if so, how did u cure it? i am genuinely interested, as i have been diagnosed with fatty liver, but i didnt think my diet was especially unhealthy, and i know fatty liver can occurr purely from genetics and not from bad diet, although im sure diet is too blame most of the time.

again. i dont know nor did i claim to know that sandra cabots book is any good or if she knows wat shes talking about. it was just something to think about.

and i too doubt hoppi has a fatty liver, he shouldnt just assume he has something without the proof. hoppis a cool guy, but definately suffers from cyberchondriasis.

imprisoned-radical wrote:

LawOfThelema wrote:i'll bet OP's ultrasound came back negative for fatty liver. MPB / forum induced hypochondriasis is a fucked up thing. guys running around every which way trying to pin their hair loss onto a general health ailment.

Well, non-alcoholic fatty liver disease pretty much implies insulin resistance and metabolic syndrome. It would be reasonable to say that there's a connection between MPB and fatty liver disease.

NAFLD is probably due to caloric excess. If you're consuming more calories than you're burning, then your liver converts sugars into fats (hence fat deposits in the liver).

Well, non-alcoholic fatty liver disease pretty much implies insulin resistance and metabolic syndrome. It would be reasonable to say that there's a connection between MPB and fatty liver disease.

Androgen receptor CAG repeat length polymorphism modifies the impact of testosterone on insulin sensitivity in men.
Möhlig M, Arafat AM, Osterhoff MA, Isken F, Weickert MO, Spranger J, Pfeiffer AF, Schöfl C.
Source

Department of Endocrinology, Diabetes and Nutrition, Charité-University Medicine Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. matthias.moehlig@charite.de

Abstract

OBJECTIVE:
Low circulating testosterone concentrations have been associated with insulin resistance (IR). Androgen action is mediated by the androgen receptor (AR) whose activity is modulated by a polymorphic CAG repeat sequence within exon 1. An interaction between testosterone and CAG repeat length (CAG length) with respect to IR has been described in women.

OBJECTIVE:
We investigated such a putative interaction between testosterone and the CAG length with respect to IR in men with normal glucose tolerance.
DESIGN:

Cross-sectional study.

METHODS:
In 113 non-diabetic men calculated free testosterone, the CAG length, and a multiplicative interaction term were investigated by multiple linear regression analysis for an association with IR, as indicated by homeostasis model assessment (HOMA %S).

RESULTS:
In a multivariate regression analysis adjusted for age and body mass index, free testosterone, CAG length, and a multiplicative interaction term were significantly associated with IR (P=0.001, P=0.001, P=0.01 respectively). The model explained 36.6% of the variation of IR and predicted that in carriers with a CAG length of 23, changes in testosterone would only minimally affect IR. For CAG lengths longer than 23, however, an increase in testosterone would improve IR, namely the longer the CAG length, the greater the effect. In contrast, in the case of CAG lengths shorter than 23, the effect of increasing testosterone would be the opposite.

CONCLUSIONS:
In men, testosterone and the AR CAG repeat length polymorphism interacted with respect to IR. The interpretation of the association between testosterone and IR seems to require consideration of the AR CAG repeat polymorphism.

abc123 wrote:

imprisoned-radical wrote:

LawOfThelema wrote:i'll bet OP's ultrasound came back negative for fatty liver. MPB / forum induced hypochondriasis is a fucked up thing. guys running around every which way trying to pin their hair loss onto a general health ailment.

Well, non-alcoholic fatty liver disease pretty much implies insulin resistance and metabolic syndrome. It would be reasonable to say that there's a connection between MPB and fatty liver disease.

NAFLD is probably due to caloric excess. If you're consuming more calories than you're burning, then your liver converts sugars into fats (hence fat deposits in the liver).

Being overweight in itself will contribute to fatty liver. However, what's interesting is that a significant proportion (30-35%) are lean individuals.

Only 20% of the fat in the liver of NAFLD actually comes from DNL; 59% comes from fatty acid influx to the liver.

Mastery wrote:ABC this is very interesting and you often post intelligently - please can you tell us more about how you believe liver health can be improved from a "a fatty liver". I'd appreciate hearing your views...