Archive for fatty liver
Risk factors for non-alcoholic fatty liver disease – (06-10-04)
Posted by: | CommentsInsulin resistance and CRP as independent risk factors for non-alcoholic fatty liver disease
I just thought I would use this article to tie in with the new documentary “Supersize Me.” This is exactly what happened to the star of this film. He ended up with elevated liver enzymes just 3 weeks into his program. The fast food had induced insulin resistance and elevated inflammation in this short a period of time.
Insulin resistance and C-reactive protein as independent risk factors for non-alcoholic fatty liver disease in non-obese Asia.
Increased prevalence of fatty liver in arterial hypertensive patients – (07-16-04)
Posted by: | CommentsIncreased prevalence of fatty liver in arterial hypertensive patients with normal liver enzymes: role of insulin resistance
See–I’m really NOT making this insulin resistance stuff up!! You would think so because it’s still ignored. Let me put it this way–in my opinion, there is no other condition that even comes close to causing the widespread damage to the human body and increases risk of death and morbidity like insulin resistance. There is no other disease with a prevalence as high as insulin resistance that is so grossly ignored. The medical literature is loaded with info and research on insulin resistance. The condition is very, very amenable to lifestyle changes.
As a summary, if the CDC, the American Diabetic Association, the American Cancer Society and the American Heart Association wanted to have the most dramatic effect on their respective diseases that they have every seen, they would make a huge marketing push to educate the general population on this condition.
Gut — Abstracts: Donati et al. 53 (7): 1020 -
GGT, A MARKER OF LIVER OR GALL BLADDER DYSFUNCTION – (11-07-05)
Posted by: | Commentsgamma-Glutamyltransferase as a Risk Factor for Cardiovascular Disease Mortality
GGT is normally thought of as a marker of liver or gall bladder dysfunction (it is called a liver “function” test, but is actually looked for dead cells spilling more of the enzymes into the bloodstream–hardly a marker of “function” if you ask me…), but has been gaining increased popularity as a marker of CVD and insulin resistance. So, chalk yet another marker up for risk of insulin resistance and CVD. One thing I have not seen mentioned, however, is whether the relationship is direct or indirect.
Insulin resistance is known to cause an elevation of liver enzymes and non-alcoholic steatohepatitis (or called non-alcoholic fatty liver disease- NAFLD). So, is this just another marker of the damage that insulin resistance is doing, or does the GGT have a direct relationship to CVD? And does it matter??
STRONG LINKS BETWEEN FATTY LIVER AND INSULIN RESISTANCE – (04-24-06)
Posted by: | CommentsLong-term prognosis of nonalcoholic fatty liver disease: Is pharmacological therapy actually necessary?
If anyone were to ask me, the lowly chiropractor, this same question, I would be hard pressed NOT to go into a long diatribe about the strong links between fatty liver and insulin resistance, and that lifestyle changes have been found in study after study to be safer, cheaper and more effective than pharmacological intervention…
PREVALENCE OF FATTY LIVER IN CHILDREN – (03-05-07)
Posted by: | CommentsPrevalence of Fatty Liver in Children and Adolescents
Well, if you’re in support of the concept that the health of our society is going to Hell in a handbasket, you’ll love this study. A staggering 13% of children aged 2-19 had fatty liver. Fatty liver. The pre-liver cirrhosis stuff. As if children did not already have the health card stacked against them from their parents’ poor health choices during pregnancy and as an infant.
Now we will have to add liver failure to the list of conditions that children are going to be getting earlier and earlier–right next to breast cancer, diabetes and heart disease.
Has natural selection in human populations produced two types of metabolic syndrome (with and without fatty liver)?
I have to admit, with as familiar as I am with metabolic syndrome, the concept that there may be three main clinical manifestations is new to me, but makes sense. We know that there are certain cells that make up the main contributors to insulin resistance and glucose metabolism: muscles, adipose tissue and liver. I’ve always viewed the effects as identical, but this author is suggesting that we may get 3 separate clinical pictures depending upon which tissue is most affected. Thinking about this and applying it to patients in my office, it makes much sense. I have very insulin resistant patients with very low body fat. I have patients that seem to have elevated liver enzymes long before anything else appears. And I have patients that look relatively lean but have a high body fat.
All these pictures would suggest different tissues being affected and may lead to different emphasis on treatments. Interestingly, the main drugs available today to treat insulin resistance in diabetics acts ONLY in the liver and would probably be minimally effective in the other two clinical scenarios presented here.
RISK INVOLVED IN OVERUSE OF ANTIBIOTICS – (01-15-07)
Posted by: | CommentsMetabolic profiling reveals a contribution of gut microbiota to fatty liver phenotype in insulin-resistant mice
Another mouse study…this one finds that a high fat diet was converted by the bacteria in the gut in such a way as to increase the risk of liver damage and increase insulin resistance. So how does this impact our GI tract when we are bombarded with nonessential antibiotics and the bacterial types that we have spent several hundred thousand years gettting acquainted with are not replaced?
The buzzword around antibiotic overuse is always antibiotic resistance, and this is, in reality, only a very small measure of the damage antibiotic overuse does to our physiology and risk of chronic diseases.
Association between Hypothyroidism and Small Intestinal Bacterial Overgrowth
Talk about the complicated web that makes up our physiology!! In this small study, it was determined that 54% patients with hypothyroidism due to autoimmune thyroiditis had small bowel bacterial overgrowth (SMBO). So what are the connections? First, we know that anti-secretory therapy for ulcers leads to bacterial overgrowth as well.
Then, we know that SMBO has been linked to fatty liver (at first seems like a stretch, but SMBO will lead to leaky gut, allowing larger molecules to get absorbed and head straight to the liver, where the liver now has to deal with the burden). We also know that a large percentage of patients with autoimmune thyroiditis have celiac disease, which further disrupts the integrity of the GI tract.
So, we end up with an upregulation of the immune system as a result of the leaky gut, increasing our likelihood of an autoimmune condition. This can be a perfect example of a feed forward cycle, where an initial disruption in physiology leads to other problems, with these “other problems” feeding back into the cycle and making the initial disruption worse!!
L-CARNITINE TREATMENT REDUCES SEVERITY OF PHYSICAL AND MENTAL FATIGUE – (05-26-08)
Posted by: | CommentsL-carnitine treatment reduces severity of physical and mental fatigue and increased cognitive functions in centenarians
L-carnitine is a substance that helps shuttle fatty acids across the mitochondrial membrane to allow them to be used for fuel. Anything that supports the function of the mitochondria is going to have positive benefits on a variety of conditions, most notably in those cell types that require high amounts of energy such as the neurons.
DIABETICS SHOULD SNACK ON THESE
Posted by: | CommentsDespite massive amounts of evidence and research on how to avoid and / or eliminate diabetes, the public still isn’t receiving the message. Sometimes small changes that are incredibly simple can make major improvements.
As an example, avoiding bottled water and switching to tea is a simple change moving from BPA loaded water to polyphenol rich tea. Avoiding all artificial sweeteners. Burst type aerobic exercise, even if it is just for 10 minutes a week.
This particular study focuses on the power of almonds to improve diabetes. The authors took “well controlled” diabetics (I personally hate that phrase–no one is ever “well controlled” if they need medication to get there) and had them eat a single serving of almonds with breakfast 5 days / wk for 4 months.
They found a massive 30% reduction in blood sugar levels and a 4% reduction in HbA1c levels in these patients, which, in some patients, may be enough to reverse the diabetes diagnosis. Few medications than can do this are without side effects.
These results are even more surprising when you take into account the standardized breakfast that the diabetics ate was bagels, butter and juice–ALL absolute no-nos for diabetics! Despite the pro-diabetic breakfast, the almonds were still powerful enough to drop HbA1c levels. How simple is that??
Two things to add..
First, raw or dry roasted almonds only. Nothing that comes out of a can or has any added oils to them. Big mistake that many make. And while this study looked at almonds, I would not be surprised to find many other nuts having similar effects.
Second, chew more. Several studies have found that by merely chewing food more we get a stronger anti-diabetic effect, especially in almonds.
If you’re diabetic, what are you waiting for? If you’re not, you should make it a habit anyway..
