KetosisMD

KetosisMD t1_jecg432 wrote

The new index, an empirical dietary inflammatory index (eDII), is based on 8 pro-inflammatory components (red meats, processed meats, organ meats, other fish, eggs, sugar-sweetened beverages, tomatoes, and refined grains) and 8 anti-inflammatory components (leafy green vegetables, dark yellow vegetables, fruit juice, oily fish, coffee, tea, wine, and beer or other alcohol beverages).

Not a fan of their definition of inflammatory.

Booze and juice ? Garbage

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KetosisMD t1_jdz1vtj wrote

> ⇒ This study demonstrates an association between atopic disease and the development of OA; patients may benefit from the use of treatments that inhibit mast cells and allergic cytokines to treat or prevent OA.

Ketotifen fumarate (Zaditen®; Swedish Orphan Biovitrum) functions as a mast cell stabiliser and has been used as a treatment for chronic idiopathic urticaria because of its antipruritic properties. Similarly, epinastine hydrochloride is both an antihistamine and a mast cell stabiliser.

Within the flavone class, the most active mast cell stabilizers are luteolin, disometin and apigenin. Using anti-IgE to elicit degranulation, luteolin inhibited the release of histamine, LTs, PG2 and GM-CSF from human cultured mast cells (HCMCs) in a concentration-dependent manner (1–100 μM) (Kimata et al., 2000b). Luteolin also suppressed the production of proinflammatory cytokines TNF-α and IL-6 in bone marrow-derived cultured murine mast cells

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3764846/

Glucosamine stabilizes mast cells as well.

https://pubmed.ncbi.nlm.nih.gov/20093129/

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KetosisMD t1_jdmhtug wrote

They used 22 protein levels to assess an aging index called SASP:

Here are the 22 proteins:

> As in our previous studies28,30, the 22 proteins included in the SASP index used in the present study are IGFBP-6, IGFBP-2, MIP-1β, IL-1β, GMC-SF, PLGF, Angiogenin, MIF-1, MIP-1α, Gro-α, IL-6, MCP-4, Gp130, ICAM-1, MCP-1, IL-8, MIP-3 α, Osteoprotegerin, TIMP-1, uPAR, TNFRI and TNFRII. The raw values were log transformed and standardized to z scores, and the SASP index for each participant was calculated

> Cellular senescence11 has emerged as a pivotal hallmark of the biology of ageing. It is a complex stress response in which cells irreversibly lose their proliferative capacity, become resistant to apoptosis12 and develop a multicomponent secretory phenotype13, referred to as the senescence-associated secretory phenotype (SASP)12. The SASP includes proteins involved in cycle control, intercellular communication, the immune-inflammatory response and tissue remodelling14. Under non-pathological conditions, SASP proteins are essential for embryonic development and tissue patterning throughout life15. However, the accumulation of senescent cells and the increased secretion of SASP proteins with age is linked to tissue deterioration and the emergence of physical disorders prevalent in older adults16. Human and animal studies found that the increased expression of SASP proteins drives multiple age-related phenotypes, such as atherosclerosis17, osteoarthritis18, cancer19, kidney dysfunction20 and a shortened health span21. In humans, an increase in SASP proteins is related to obesity, cardiometabolic dysregulation22 and frailty14. Several studies characterized the role of cellular senescence and SASP proteins in the brain. Aged microglia, astrocytes and neurons exhibit various features of senescence, including the expression of SASP proteins23,24,25.

> While the cellular source of SASP proteins is unknown, some evidence suggests that the SASP index is relevant to brain health and that brain cells express SASP proteins23,24,25. In ageing and psychiatric disorders, the blood–brain barrier permeability is increased71, leading to an enhanced passage of proteins. Some studies suggest that plasma from old mice accelerates brain ageing in young mice72, and senolytic interventions targeting the periphery alleviate the effect of SASP proteins on the brain71.

Unknown !

Blood brain barrier permeability increased.

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KetosisMD t1_jbgcq8d wrote

People lost 4 lbs in 3 months eating the low carb bread. People over 55 lost 5 lbs.

> The rye bread was made from type 997 flour, the low-insulin-stimulating bread consisted of oat flakes, sunflower seeds, flax seeds, chia seeds, psyllium husks, chopped almonds, baker’s honey, and Rhinish field beans

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KetosisMD t1_j7iwutt wrote

Too much D lowers folic acid.

This paper says sun (ultraviolet rays) exposure Lowers folate not vitamin D

> Vitamin D and folate are two unrelated nutrients with disparate sensitivities to UVR; vitamin D is synthesised and folate is degraded in the skin following UVR exposure.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986434/

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KetosisMD t1_j7i14jt wrote

That’s nuts.

I can’t believe anyone prescribed dangerous placebos.

It’s hard to know what is more broken the FDA or Healthcare

Edit

> 1.5 million treated

No, 1.5 million would be eligible. CMS denied coverage to anyone who isn’t in a trial.

This is good news. I was hoping CMS would pass on this drug and they did.

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KetosisMD t1_j49fysl wrote

Love your post. Knowledge is power.

Thoughts on this ?

https://www.crossfit.com/essentials/insulin-is-not-required-for-glucose-uptake-into-cells

> get glucose intake to match glucose-independent uptake

If blood glucose was stable and it went up 18mg/dl (1 mmol) wouldn’t that indicate the intake was too high ?

1

KetosisMD t1_j3qy8k1 wrote

> salt

The evil white powder is sugar.

Sugar spikes insulin and causes salt retention.

No sugar = just pee out the salt.

Nothing wrong with lowering salt intake, but the killer white powder is sugar.

Final answer.

> reformulate packaged food.

ahem, eliminate.

You know something is bad for you if it has a nutrition label

Processed food is just sugar, salt, low quality oil and wheat. Lowering salt in fake food isn’t going to do much.

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