P.S. The censors came after Mercola, and he took much of his content off-line, including my video.
For new visitors, here are a few of my key posts, some of which are mentioned in the interview.
Below are the extremely rough notes that Dr. Mercola and I worked off in the interview, including a bibliography.
Questions are welcome in the comments.
Why this is likely the major reason contributing to metabolic dysfunction
and the epidemic of chronic disease
Criteria that I concluded had to be true for the cause
(whatever it was) of chronic disease.
1. Trans-Species
This is a problem that we see in all human populations, and the animal species
that associate with them, which includes pets but also feral animals like rats,
pigeons, and racoons.
This eliminates genetic causes, and many pathogens, which do not cross species
lines easily.
2. Diet-based
Several crucial books (Price,
1938; Stefansson, 1960; Trowell & Burkitt, 1981) looked at healthy,
traditional cultures compared to sick ones, and made a clear suggestion that it
was diet based T&B made it clear that it affected diseases seemingly
unrelated to diet, like auto-immunity.
This eliminates other proposed mechanisms, like pollution (fattest country on
earth is in the South Pacific: what is the pollution?).
3. Novel
Must be a food that was recently introduced, contemporaneously with the
emerging pandemics of T2DM and obesity. (Taubes,
2008) looked at diabetes emergence in the 1800s, (Lee
et al., 1964) looked at emergence of ischaemic heart disease in the 20th
century vs traditional cultures.
4. Mechanistic
confirmation
Too easy to be fooled by epidemiology without some mechanistic
confirmation, as happened to Ancel Keys. (Ramsden
et al., 2016)
5. Contained
in D12492
This is the diet used to induce chronic diseases in lab animals. It seems
silly, but no-one went through this diet to figure out what ingredient actually
had the measured effect until 2012!
How you figured this out so early
Jen’s explanation (more complimentary): "Always
open-minded and not biased as to what other people were believing and the
trends. Simply were assessing evidence-based research and making decisions
according to that."
My version: "Dumb luck and stubborn."
Had dramatic personal experience that couldn’t be explained
by physicians, so looked into why it had happened. Stuck with exploration even
when mentor in topic abandoned it.
Some seminal studies that provide irrefutable evidence of the hypothesis
“Irrefutable” is hard, if such a study had been done you
wouldn’t be talking to me, this would be old news. Must follow Bill Lands, a
pioneer in PUFA research, and “connect the dots”.
(Alvheim
et al., 2012) shows what induces obesity, explains mechanism behind
human-approved drug that treated multiple aspects of chronic diseases. Compare
to D12492.
“Large randomized trials with rimonabant have demonstrated
efficacy in treatment of overweight and obese individuals with weight loss
significantly greater than a reduced calorie diet alone. In addition, multiple
other cardiometabolic parameters were improved in the treatment groups
including increased levels of [HDL], reduced triglycerides, reduced waist
circumference, improved insulin sensitivity, decreased insulin levels, and in
diabetic patients improvement in [HbA1c].” (Bronander
& Bloch, 2007)
(Medina-Navarro
et al., 2003) showing a physiological level of glucose and PUFA produced a
poison in vitro. My tweet: “
Etiology of metsym &
chronic disease, in one chart. At physiologic lvls. God...”
(Singh
et al., 2008) “Fat accumulation in Caenorhabditis elegans triggered by
the electrophilic lipid peroxidation product 4-hydroxynonenal (4-HNE). Tweet: “N-6
metab 4-HNE induces obesity across species, "the process is conserved and
thus likely to be universal."”
(Liu
et al., 2011) “Formation Of 4-Hydroxynonenal From Cardiolipin Oxidation:
Intramolecular Peroxyl Radical Addition And Decomposition”
(Witztum
& Steinberg, 1991)
(Ghosh
et al., 2004) “Brief episode of STZ-induced hyperglycemia produces cardiac
abnormalities in rats fed a diet rich in n-6 PUFA” (Goodrich,
2018)
(Skulachev
et al., 2009) “An attempt to prevent senescence: A mitochondrial approach”
(Bethancourt
et al., 2019) “Household use of cooking oil increased and was positively
associated with female BMI. Consumption of domesticated animal products did not
change significantly but was positively associated with female BMI and male
waist circumference. Conclusions Even small increases in energy-dense
market-based foods can contribute to adiposity gains among a moderately active,
subsistence-based population.”
(Maciejewska
et al., 2015) “Following the six-month dietary intervention, hepatic steatosis
resolved completely in all patients. This resulted in a significant decrease in
the concentrations of all eicosanoids (LX4, 16-HETE, 13-HODE, 9-HODE, 15-HETE,
12-HETE, 5-oxoETE, 5-HETE) and key biochemical parameters (BMI, insulin,
HOMA-IR, liver enzymes).”
(Goodrich,
2016) “The Cause of Metabolic Syndrome: Excess Omega-6 Fats (Linoleic Acid) in
Your Mitochondria”
Will dive a bit into cardiolipin as I believe that is a major reason to
explain the dilemma
Yes, covered in links above, plenty of material for discussion
Your best guess as to ideal LA consumption for optimal health and how to do
that
LA is not essential, despite what was thought over last 90
years. Consumption should be minimal, discuss what should be avoided. (Alvheim
et al., 2013; Blasbalg et al., 2011; Carlson et al., 2019)
Can tangent a bit to carnosine as a way to supply a sacrificial scavenger
for reactive carbonyl species (RCS) or in LA context better known as OXLAMs or
oxylipids
(Nègre-Salvayre et al., 2017) “A recent study
by Colzani and colleagues analyzed and compared the ability of several
classical carbonyl scavengers to prevent the carbonylation of proteins, and
concluded that carnosine is the most effective scavenger for HNE...”
(Zhao
et al., 2015) “Carnosic Acid as a Major Bioactive Component in Rosemary Extract
Ameliorates High-Fat-Diet-Induced Obesity and Metabolic Syndrome in Mice”
References
Alvheim,
A. R., Malde, M. K., Osei‐Hyiaman, D., Hong, Y. H., Pawlosky, R. J.,
Madsen, L., Kristiansen, K., Frøyland, L., & Hibbeln, J. R. (2012). Dietary
Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity. Obesity,
20(10), 1984–1994. https://doi.org/10.1038/oby.2012.38
Alvheim, A. R., Torstensen, B. E., Lin, Y. H.,
Lillefosse, H. H., Lock, E.-J., Madsen, L., Hibbeln, J. R., & Malde, M. K.
(2013). Dietary linoleic acid elevates endogenous 2-arachidonoylglycerol and anandamide
in Atlantic salmon (Salmo salar L.) and mice, and induces weight gain and
inflammation in mice. The British Journal of Nutrition, 109(8),
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Bethancourt, H. J., Leonard, W. R., Tanner, S., Schultz,
A. F., & Rosinger, A. Y. (2019). Longitudinal Changes in Measures of Body
Fat and Diet Among Adult Tsimane’ Forager-Horticulturalists of Bolivia,
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https://doi.org/10.1002/oby.22556
Blasbalg, T. L., Hibbeln, J. R., Ramsden, C. E.,
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cardiometabolic risk: A narrative review of available data. Vascular Health
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Chang, M., Cowan, E., Mitchell, P. D., Gura, K. M., Fagiolini, M., & Puder,
M. (2019). A Diet With Docosahexaenoic and Arachidonic Acids as the Sole Source
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Ghosh, S., Qi, D., An, D., Pulinilkunnil, T.,
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Rodrigues, B. (2004). Brief episode of STZ-induced hyperglycemia produces
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Goodrich, T. (2018, June 28). What’s Worse—Carbs or
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http://yelling-stop.blogspot.com/2018/06/whats-worsecarbs-or-seed-oils.html
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