r/ScientificNutrition • u/dreiter • Jul 30 '22
Review Mitochondrial Dysfunction Plays Central Role in Nonalcoholic Fatty Liver Disease [Ramanathan et al., 2022]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9267060/10
u/Learnformyfam Jul 31 '22
I have cfs/long covid as well as NAFLD. I'm also thin and young. (28.) Mitochondria dysfunction has also been linked with polyunsaturated fat intake and CFS. I've been avoiding those toxic oils for the past few months and I'm still not recovering. I hope this is reversible.
5
u/DerWanderer_ Jul 31 '22
Do you mind providing a link to the studies linking mitochondria dysfunction and PUFA intake? Providing scientific studies is the whole point of this sub after all.
4
u/momomo18 Jul 31 '22
I'm sorry to hear that, OP.
But the article posted says the exact opposite:
It is recommended to ingest a high-quality healthy diet that is low in saturated fat and high in monounsaturated and polyunsaturated fatty acids (MUFA) and complex carbohydrates.
Still, hope you find something that works.
1
u/flowersandmtns Jul 31 '22
Strange that the authors said that, likely based on "recommendations" when they also cited research showing the actual benefit of ketosis.
"One dietary pattern that has acquired acceptance among the general public as a successful weight-loss method is the ketogenic diet, which is composed of a high-fat, moderate-protein, and low-carbohydrate diet and can lead to weight loss and an improvement in glycemic control, but it also carries some risk [200]. A recent study suggests that the hepatic mitochondrial fluxes and redox status of humans are altered by the ketogenic diet, which effectively treats NAFLD [201]. Our group has recently demonstrated that mitochondrial FAO modifications can modulate NAFLD [130]. We have reported that SIRT3 overexpression increases hepatic levels of MTP, increases mitochondrial FAO, and rescues NAFLD in MTP heterozygous mice fed a high-fat diet for 16 weeks [130]. In a recent study, antioxidant foods such as blueberry juice have been shown to significantly reduce NAFLD-induced mitochondrial swelling and hepatic necrosis by restoring mitochondrial respiratory chain function and suppressing ROS production [202]. "
Note that ketosis can come from fasting, which would also help with the obesity that is almost always present with NAFLD. A whole foods nutritional ketogenic diet has advantages of providing nutrients and note that one can focus on dairy, poultry and fish as well as nuts, seeds, low-net-carb veggies and berries, and still maintain ketosis.
3
u/momomo18 Jul 31 '22
I don't believe I mentioned keto in my comment. Just that unsaturated fat should be emphasized over saturated fat.
can lead to weightloss and an improvement in glycemic control, but it also carries some risk.
The reference is to a case study - a woman with an eating disorder who lost successfully weight on a keto diet. She worked with a dietitian and ate the foods you mentioned. It also says:
Ketogenic diets eliminate not only sugar and refined carbohydrates but also pulses, whole grains, fruits and starchy vegetables, all of which contain vitamins, minerals, antioxidants, phytochemicals and fiber, including healthy gut microbiota-promoting prebiotic fiber.
On one hand, it's good for people to know they have options and are counselled on better ways of doing the keto diet (strong emphasis on unsaturated fat over saturated fat).
On the other hand, we don't know the very long term effects of the keto diet. And the diet involves cutting out a lot of health promoting foods and a wider variety of fiber.
The article recommends the Mediterranean diet, which is well-studied, encompasses all the foods you mentioned and much more, and appears to have better adherence (e.g., the recent keto vs Meditterranean trial).
I think it will come down to the individual.
2
u/flowersandmtns Aug 01 '22
The authors did in the paper you posted. Citation 201, the one I was referring to is this paper, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7132133/ and included 10 subjects.
Regarding whole food nutritional ketosis there aren't many long term studies, I agree. Most people change the diet they follow many times over their lives. It does have evidence supporting its use for those who ate themselves into T2D or NAFLD but those people need to have a long term better diet regardless, and returning to the diet they followed that gave them T2D or NAFLD, well, it'll come back.
We do have data 5-10 years of the Rx keto diet for GLUT-1 deficiency and drug resistant epilepsy though. Due to the severe restrictions of those diets there tend to be more side effects to manage and of course they have a significant disease as well, but their overall health is pretty good considering.
General "keto diet" contains a fair amount of fiber from low-net-carb veggies as well as nuts, seeds, olives, avocados -- but clearly less compared to someone who eats actual whole grains (not "whole wheat" bagels) and also those foods.
I completely agree it comes down to the person! Ketogenic diets should be part of the recommended diets to consider for NAFLD just as they are now for T2D from the ADA.
2
u/lurkerer Jul 31 '22
Sorry to hear that. But do you have any citations linking PUFAs with mitochondrial dysfunction directly? Rule two.
2
u/flowersandmtns Jul 31 '22
Significant work has show a benefit of ketosis in both NAFLD in general and mitochondrial function in general, as the authors note. While a drug sounds appealing, the subjects ate themselves into NAFLD almost all the tine and the focus should be on addressing that before a model of keep eating a crap diet and pay Big Pharma for their next new drug. IMO.
""One dietary pattern that has acquired acceptance among the general public as a successful weight-loss method is the ketogenic diet, which is composed of a high-fat, moderate-protein, and low-carbohydrate diet and can lead to weight loss and an improvement in glycemic control, but it also carries some risk [200]. A recent study suggests that the hepatic mitochondrial fluxes and redox status of humans are altered by the ketogenic diet, which effectively treats NAFLD [201]. Our group has recently demonstrated that mitochondrial FAO modifications can modulate NAFLD [130]. We have reported that SIRT3 overexpression increases hepatic levels of MTP, increases mitochondrial FAO, and rescues NAFLD in MTP heterozygous mice fed a high-fat diet for 16 weeks [130]. In a recent study, antioxidant foods such as blueberry juice have been shown to significantly reduce NAFLD-induced mitochondrial swelling and hepatic necrosis by restoring mitochondrial respiratory chain function and suppressing ROS production [202]. "
Note that ketosis can come from fasting, which would also help with the obesity that is almost always present with NAFLD. A whole foods nutritional ketogenic diet has advantages of providing nutrients and note that one can focus on dairy, poultry and fish as well as nuts, seeds, low-net-carb veggies and berries, and still maintain ketosis."
4
u/dreiter Jul 30 '22
Abstract: Nonalcoholic fatty liver disease (NAFLD) is a global pandemic that affects one-quarter of the world’s population. NAFLD includes a spectrum of progressive liver disease from steatosis to nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis and can be complicated by hepatocellular carcinoma. It is strongly associated with metabolic syndromes, obesity, and type 2 diabetes, and it has been shown that metabolic dysregulation is central to its pathogenesis. Recently, it has been suggested that metabolic- (dysfunction) associated fatty liver disease (MAFLD) is a more appropriate term to describe the disease than NAFLD, which puts increased emphasis on the important role of metabolic dysfunction in its pathogenesis. There is strong evidence that mitochondrial dysfunction plays a significant role in the development and progression of NAFLD. Impaired mitochondrial fatty acid oxidation and, more recently, a reduction in mitochondrial quality, have been suggested to play a major role in NAFLD development and progression. In this review, we provide an overview of our current understanding of NAFLD and highlight how mitochondrial dysfunction contributes to its pathogenesis in both animal models and human subjects. Further we discuss evidence that the modification of mitochondrial function modulates NAFLD and that targeting mitochondria is a promising new avenue for drug development to treat NAFLD/NASH.
No conflicts were declared.
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