I've been reading some posts over the past few days and some people around here were saying that saturated fat is harmless, it's the high carb that really damages people. I would agree that high carb is bad for you, but I would also say, watch how much saturated fat you are getting. I generally keep my saturated fat level below 10g a day, majority of fat is unsaturated and some polyunsaturated

Read this new tudy below:

Fat Overload Kills Mammalian Cells -- Key Culprit Identified

http://www.sciencedaily.com/release...60118210500.htm

Investigating the harmful health effects of excess fat, researchers at Washington University School of Medicine in St. Louis have identified a protein that triggers death in mammalian cells overloaded with saturated fat.

The internal "skeleton" (in red) of cells is altered by exposure to high fat.

When the researchers halted production of this protein, called EF1A-1, the cells were able to thrive in ordinarily damaging amounts of the saturated fat palmitate, a fat abundant in Western diets. At the same concentration of palmitate, normal cells still producing EF1A-1 rapidly died. The study will be published in the February 2006 issue of Molecular Biology of the Cell.

"When lipids (fats) accumulate in tissues other than adipose tissue, cellular dysfunction or cell death results," says senior author Jean Schaffer, M.D., associate professor of medicine and of molecular biology and pharmacology. "For example, preliminary studies on animals suggest that the accumulation of fat in the pancreas contributes to the development of diabetes, and accumulation of lipids in skeletal muscle of leads to insulin resistance."

Other studies have linked the genesis of heart failure to fat-induced cell dysfunction and cell death in the heart. "As physicians our primary focus in diabetic patients is on glucose control," says Schaffer, a member of the Center for Cardiovascular Research at the School of Medicine and a cardiologist at Barnes-Jewish Hospital. "But it appears we should also be more aggressive with respect to lowering lipids such as triglycerides and fatty acids."

With the discovery of EF1A-1's role, this study is the first to identify a critical step in the pathway that leads from high cellular fat to cell death, according to Schaffer. EF1A-1 is an extremely abundant protein with several diverse functions within cells, including protein synthesis and maintenance of the cytoskeleton, the cell's internal support structure.

In mammalian cells grown in culture, the researchers saw that EF1A-1 and the fat palmitate work hand in hand: the presence of EF1A-1 dictated sensitivity to palmitate-induced cell death, and palmitate caused a rapid increase of the amount of EF1A-1 produced.

Schaffer's laboratory earlier had developed a transgenic mouse that accumulates fat in its heart muscle cells resulting in the death of cells, heart failure and premature death. They found that EF1A-1 was increased nearly three-fold in the hearts of these animals.

Removal of EF1A-1 protected cells from palmitate-induced death, and its absence allowed cells to withstand assault by highly reactive oxygen molecules. According to study authors, this indicates that EF1A-1 probably contributes to cell death from oxidative stress, which is known to stem from high lipid levels. Cytoskeletal changes seen in cells missing EF1A-1 suggested to the researchers that EF1A-1's cytoskeletal role also is important in cell death resulting from fat overload.

"Cells have a lot of mechanisms for incorporating fatty acids into storage forms, for metabolizing them or for using them in cellular membranes," Schaffer says. "But saturated fats like palmitate are poorly stored in the tiny fat droplets normally found in most cells and therefore are more likely to enter into pathways that lead to cell death such as the one in which EF1A-1 is involved."

In the process of identifying the role of EF1A-1, the lab members uncovered other proteins implicated in the toxicity of excess fats. They are now investigating each to find out what part it plays.

Future investigations by Schaffer's research team will study the EF1A-1 protein to see whether fatty molecules directly alter the protein, or if they cause it to relocate within the cell.

Borradaile NM, Buhman KK, Listenberger LL, Magee CJ, Morimoto ETA, Ory DS, Schaffer JE. A critical role for eukaryotic elongation factor 1A-1 in lipotoxic cell death. Molecular Biology of the Cell, February 2006.

Funding from the National Institutes of Health, the Washington University School of Medicine--Pharmacia Biomedical Program (JES) and the Heart and Stroke Foundation of Canada supported this research.

The study was done on cells grown in a culture doped with palmitate... so explain how this has anything to do with dietary fat. Fat accumulation in muscle and organs is the result of high-carb intake producing high levels of blood triglycerides.

Wyv

Whoa,
A common logical mistake (when it comes to nutrition especially) is to assume things happen very very simply in a direct cause/effect relationship. For example, women think if they eat a bag of twizlers that say "fat free" it will help them lose fat (because if you don't eat fat, you won't be able to store fat). Or, men often buy expensive designer protein powders because they think consuming gross quantities of protein will encourage their body to build more muscles. Just the other day a study was posted which showed fatty acid levels in the hypothalamus have a powerful affect on appetite; numerous people seemed to assume that eating fat controlled this process (when, in fact, it may have nothing to do with it since the body manufactures fatty acids on its own... it's much more likely the entire metabolic state affects hypothalamic fatty acid levels).

It seems that's what you're doing here. This study shows that (saturated) fat accumulation (in viscera/organs) -> cellular death -> disease -> organism death. You (and most people I'm sure) will conclude that it is unwise to consume staurated fat.

However, the reality is consuming saturated fat, this isolated variable, has nothing to do with the accumulation of visceral/organ fat. It is often metabolic disease and hyperinsulinemia which is the real direct cause of buildup of visceral fat. We all know that diets which are excessively high in carbohydrate, refined carbohydrates, and calories lead to the hyperinsulinemic/metabolic syndrome constellation of disorders. We also know that increasing saturated fatty acid consumption, while simultaneously adopting an unrefined carbohydrate restricted plan, leads to dramatic improvements in body fat (visceral fat too) and metabolic syndrome.

So, ironically and as unseemingly as it is, it is carbohydrate that is the real culprit here. Restricting saturated fat to reduce visceral fat is as worthless as restricting dietary cholesterol to improve blood lipids. Both of these metabolic symptoms are the result of metabolic disease. It is a disease caused by poor diet, lack of exercise, excessively high carbohydrate and calories (although the calorie issue is often redundant once the disease is addressed by moving a bit more and dropping the white death from your diet)

Oh and by the way, it is unwise to consume a preponderance of polyunsaturated fatty acids. Their molecular structure renders them highly reactive with light and heat. This means they become "deformed" easily, producing toxic byproducts (free radicals) that drain our body of antioxidants (such as vitamine E), and damage cells. PUFAs contribute to aging greatly, which is something you as a CRONer should be concerned with. Ironically, you should be careful to select cold pressed oils made up primarily of monosaturates and saturates.

I agree with Wyvrn. Palmitate is the principal fatty acid produced by de novo lipogenesis, the process by which the liver converts glucose into fat for storage as adipose tissue. So the results of this study have nothing to do with any fat that we eat. The way to avoid palmitate is very clear: eat low carbohydrate and keep insulin levels low.

So, Whoa182, avoiding saturated fat in the diet will have absolutely no effect on what the researchers are reporting about cell death. Polyunsaturated fat is the stuff to avoid. The fact that the researchers focused on a particular protein to overcome cell death means that they're looking for a drug to sell. Don't trust this research.

Ok, that is how I read it to. If you get fat, cells die. Not if you eat fat.

The reason that overweight people have too much fat in their cells is from eating carbs. The excess glucose gets converted into 100% saturated fat that has to be put somewhere. Natural sources of fat are a mixture of mono, poly and satuated fats. Even lard has more monosaturated fats than it has saturated fats.

The only thing that even begins to bring dietary SFA in to this is this quote:


But, like others and I said, carbohydrate is basically like a "SFA/palmitate seed". Eating it is like planting that seed. Even if you eat a highly saturated fat piece of meat, it's probably still not as bad as eating the pasta side dish (which will cause a hyperinsulinemic state and lead to visceral fat buildup). The fact that so many of us improve and reverse our metabolic syndrome eating this way is evidence of that...

All this is informative but leaves me befuddled!

Would someone please "bottom line" it-- i.e., give us a basic "fat" explanation (saturated, poly, mono, etc), what fats we SHOULD consume, the percentages of each and what foods to eat to manage our fat consumption.

Thanks ever so much!!

Sunrise

No one can bottomline it for you because no one really knows the answer.

My advice would be:
+Don't be afraid of saturated fats, they're healthy.
+Lower fat intake if you're stalled

You'll have to experiment yourself and see what agrees with you and what is required to lose weight.

Sunrise02 - Do a Google search on Mary Enig. She has several articles on this subject, all of which are worth reading nad very informative.

Trans-fats be bad.

LOl--yep--I got "trans fats be bad" concept!

But, coming from a "lowfat" brainwashed lifetime--it thows me into a panic when I look at my "calorie totals" at the end of the day and they are 65 F/30P/5C. Then I look at the fat distribution and see all those saturated fats. EEEKKKK!! Then, it is not only the FAT that scares me--then I see all those "saturated" fats and think--"Accckk!! Is this right?!"

Thanks for the Mary Enig info--I will look it up!

Sunrise

For the majority the year I've been consuming mostly MUFA's. I realise that Saturated fat is much more stable, Only a little of my total fat intake comes from PUFA anyway.

I 100% agree with you that high carb is a big problem, I have read many studied showing this, people do think that cutting out fat from their diet will lower their cholesterol, but that isn't the case and can even raise levels.

I am not convinced that large quantities of saturated fat is harmless, based on the number of studies done over the years. Saying that, here is a study that I just read about

Low-carbohydrate diets reduce heart disease risk, researcher finds
http://www.advance.uconn.edu/2006/060123/06012310.htm

I consume around 60g of of fat a day, mostly unsaturated. I use EVOO and keep it in a really cool and dark place, so hopefuly it should minimize oxidation!

But in a person that does CR, antioxidant enzymes like catalase are increased by as much as 50%. Which would certainly help

HS-CRP - Marker of Inflammation

Has anyone here that consumes large amount of saturated fat and been on low carb for atleast 1 year had their CRP tested? If so, what was it? I know that High glycemic foods and trans fats can increase CRP and just read a study that showed that one per cent rise in the intake of saturated fat can translate into a 0.15 per cent increase in the CRP levels.

My CRP level is now at 0.27


Also I'm really new here, so how many grams of saturated fat would a perosn on atkins typically consume daily?

Thanks

matt

Satfat is only bad when eaten in excess, AND in conjunction with a high carb diet. No studies have ever shown that satfat is bad when eaten as part of a low carb regimen.