Beige Food Four
Mitochondria and Food
“Mitochondria play a key role in both health and disease. Their function is not limited to energy production but serves multiple mechanisms varying from iron and calcium homeostasis to the production of hormones and neurotransmitters, such as melatonin. They enable and influence communication at all physical levels through interaction with other organelles, the nucleus, and the outside environment. The literature suggests crosstalk mechanisms between mitochondria and circadian clocks, the gut microbiota, and the immune system. They might even be the hub supporting and integrating activity across all these domains. Hence, they might be the (missing) link in both health and disease.”
“What Is the Function of the Mitochondria?
Mitochondria import thousands of proteins through two membranes to fulfill a variety of mitochondria functions including, but not limited to:
· Converting food into energy
· Powering a cell’s molecule production
· Managing cell death
· Regulating aging” [2]
Problematically most studies on food and either primary or secondary mitochondrial disease are awash in confusing correlations with causation. Most of the literature on ultra-processed foods involve healthy subjects and are therefore inapplicable to those with pre-existing conditions. Secondary mitochondrial impairment or disease is present for a vast array of chronic conditions from heart disease to diabetes, MS, lupus, ME/CFS, long Covid, Ehlers-Danlos, you name it…
This review in Yale Medicine made me smile as a quintessential example of the cultural skew that conflates often weak correlations with some kind of unsubstantiated causation:
“Many of the studies of ultraprocessed foods examined in the BMJ review were based on surveys and other less rigorous methods, but there was one high-quality randomized controlled study, Dr. Imaeda notes. [Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake] published in 2019, involved 20 healthy, overweight adults staying in a medical facility…”
Is the data of 20 subjects who undergo two weeks on an ultra-processed diet and two weeks on an unprocessed diet (with a washout period before cross-over) really high-quality? The researchers answer that question themselves in their “limitations of the study” section in the paper:
“…the inpatient environment of the metabolic ward makes it difficult to generalize our results to free-living conditions.”
Additionally, as I’ve already stated, healthy subjects won’t yield transferable data for those with existing conditions. “High quality” is in the eye of the beholder.
The Research Landscape of Chronic Disease and Diet
Even though many conditions present with unexplained weight loss as a telltale symptom: MS, ME/CFS, long Covid, diabetes, arthritis, heart disease, lupus, Ehlers-Danlos…the literature often focuses on weight management as a way to manage symptoms for all of these conditions. Keep in mind that restricting food intake is seen as a viable way to manage weight and it is not (see all the articles under the menu item Fat above).
Of course, unexplained weight gain with any of these conditions is also possible. Unfortunately, that feeds into cultural dogma that the act of losing weight purposefully will somehow improve the symptom expression and progression of these conditions. That is not the case. The following conclusion was drawn in 2022 for a systematic review and meta-analysis on lifestyle interventions and weight management for systemic lupus erythematosus (lupus):
“The results showed that different protocols of exercise intervention or diets were not effective to reduce body weight in patients with SLE.”
This finding shows that not only did the all the studies reviewed within that systematic review not show any correlation between weight loss and symptom alleviation or improvement, but no weight loss was achieved in the first place.
For something like multiple sclerosis (MS), the preponderance of the literature looks at dietary supplementation (B12, D vitamins etc.) and fewer studies look at weight management. One systematic review and meta-analysis looked at waist circumference and disease progression in patients with multiple sclerosis (MS). They found a correlation between higher waist circumference and more severe disease progression.[6] The problem with that correlation is most researchers and laypeople alike assume the links read in linear fashion as follows: eat bad stuff, then get a bigger waistline, then have worse disease outcomes. However, these correlations could go in the opposite direction just as easily: the person has a more severe case from the outset, then they require more energy for the body to navigate the symptoms and that drives the individual to seek out foods that provide more net energy so that the waist circumference (i.e. the fat organ) might enlarge to produce more energy modulating and extracting hormones to support mitochondrial function. It’s also just as possible that neither linear scenario captures any of the causes involved in the facets being studied here.
In a longitudinal and prospective analysis, one study found that people with TD1 consumed more ultra-processed foods than the non TD1 cohort.[7] Their concluding remarks have nothing to do with the study:
“Positive associations between UPF [ultra-processed food] consumption and obesity indicators suggest that limiting UPF can be recommended for obesity prevention and management. Further research is needed to confirm these findings.”
What findings? They weren’t studying ‘obesity’ prevention and management at all. What of the possibility that people with TD1 naturally consume ultra-processed foods at a higher rate than the non-TD1 controls because, over time it turns out mitochondrial dysfunction is part and parcel of the progression of TD1?[9] Most chronic conditions develop secondary mitochondrial dysfunction over time, if not immediately upon the appearance of the condition.
Next section available November 21.
Image in outline preview: Flickr.com Rafael Edward
Casanova A, Wevers A, Navarro-Ledesma S, Pruimboom L. Mitochondria: It is all about energy. Frontiers in physiology. 2023 Apr 25;14:1114231.
https://medschool.ucla.edu/news-article/mitochondria-function-form-and-food
https://www.yalemedicine.org/news/ultraprocessed-foods-bad-for-you
Hall KD, Ayuketah A, Brychta R, Cai H, Cassimatis T, Chen KY, Chung ST, Costa E, Courville A, Darcey V, Fletcher LA. Ultra-processed diets cause excess calorie intake and weight gain: an inpatient randomized controlled trial of ad libitum food intake. Cell metabolism. 2019 Jul 2;30(1):67-77.
Goessler KF, Gualano B, Nonino CB, Bonfá E, Nicoletti CF. Lifestyle interventions and weight management in systemic lupus erythematosus patients: a systematic literature review and metanalysis. Journal of Lifestyle Medicine. 2022 Jan 31;12(1):37.
Giannopapas V, Stefanou MI, Smyrni V, Kitsos DK, Kosmidou M, Stasi S, Chasiotis AK, Stavrogianni K, Papagiannopoulou G, Tzartos JS, Paraskevas GP. Waist circumference and body mass index as predictors of disability progression in multiple sclerosis: a systematic review and meta-analysis. Journal of Clinical Medicine. 2024 Mar 18;13(6):1739.
Pang T, Gray HL, Alman AC, Buro AW, Basu A, Lu S, Snell-Bergeon JK. Ultra-processed food consumption and obesity indicators in individuals with and without type 1 diabetes mellitus: a longitudinal analysis of the prospective Coronary Artery Calcification in Type 1 Diabetes (CACTI) cohort study. Public Health Nutrition. 2023 Aug;26(8):1626-33.
ibid.
Blake R, Trounce IA. Mitochondrial dysfunction and complications associated with diabetes. Biochimica et Biophysica Acta (BBA)-General Subjects. 2014 Apr 1;1840(4):1404-12.
