Inhibiting Hypoxia Biomarker (HIF-1) Reverses Parkinson Disease

[Hans]

@Hans I got this quote from my diagnostic lab-

DHEA (RIA) - P8,000 = $160
DHEAS (CMIA) - P2,500 = $50

Would the DHEAS test be useful?

Yes as it's the storage form of DHEA, so it will give you a good indication of long term DHEA levels and stress.

 

[yerrag]

Yes as it's the storage form of DHEA, so it will give you a good indication of long term DHEA levels and stress.

Thanks. I was looking into the reference range and it has many classifications, by age and sex, from day-old infants to seniors.

Interesting how the reference range changes, for example:

Male-

11y-15yrs: 0.50 - 6.60 umol/L
15 -20yrs: 1.2- 2.40
20-25yrs: 6.50-14.60
25-35yrs: 4.60-16.10
35-45yrs: 3.80-13.10
45-55yrs: 3.70-12.10
55-65yrs: 1.30-9.80
65-70yrs: 6.20-7.70

Are there optimal values that don't rely on age?

 

[yerrag]

Yes as it's the storage form of DHEA, so it will give you a good indication of long term DHEA levels and stress.

Thanks. I was looking into the reference range and it has many classifications, by age and sex, from day-old infants to seniors.

Interesting how the reference range changes, for example:

Male-

11y-15yrs: 0.50 - 6.60 umol/L
15 -20yrs: 1.2- 2.40
20-25yrs: 6.50-14.60
25-35yrs: 4.60-16.10
35-45yrs: 3.80-13.10
45-55yrs: 3.70-12.10
55-65yrs: 1.30-9.80
65-70yrs: 6.20-7.70

Are there optimal values that don't rely on age?

 

[Hans]

Thanks. I was looking into the reference range and it has many classifications, by age and sex, from day-old infants to seniors.

Interesting how the reference range changes, for example:

Male-

11y-15yrs: 0.50 - 6.60 umol/L
15 -20yrs: 1.2- 2.40
20-25yrs: 6.50-14.60
25-35yrs: 4.60-16.10
35-45yrs: 3.80-13.10
45-55yrs: 3.70-12.10
55-65yrs: 1.30-9.80
65-70yrs: 6.20-7.70

Are there optimal values that don't rely on age?

At the high end of the natural range for 25-35 would probably be optimal. DHEA shouldn't decrease with age.

 

[yerrag]

At the high end of the natural range for 25-35 would probably be optimal. DHEA shouldn't decrease with age.

Damn! Those reference ranges are way off!

 

[Hans]

Damn! Those reference ranges are way off!

Lol yeah. DHEA is about 10% of youthful levels in old age. That's a massive drop.

 

[yerrag]

Lol yeah. DHEA is about 10% of youthful levels in old age. That's a massive drop.

According to Life Extension, DHEA-S measurement is preferable to DHEA, as it gives a more stable reading not subject to diurnal variation. Life Extension only has DHEA-S available. Good thing!

 

[yerrag]

The elevated LDH isn't accompanied by high levels of hsCRP or ESR. In fact my hsCRP, at 0.8 is low, and my ESR, is at 0. This, to me, discounts the tissue destruction nature of my elevated LDH reading. My last LDH reading, at 221 u/L, is barely within range of 135-225, but is slightly above optimal range. It is for this reason that I believe the elevated LDH merely reflects higher LDH due to hypoxia in my kidney capillaries.

It turns out at hsCRP of 0.8 isn't that low. According to Dr. Thomas Lewis, in his book "Uncovering Chronic Inflammation and Hidden Infections: The Untold Story Behind Chronic Disease Prevention and Reversal," the cutoff value is 0.6. I didn't pay much attention to it, but here's a research article that shows that supports the idea: HS-C Reactive Protein and Red Blood Cell Width as Effective Markers for Hypertension:

 

[Hans]

It turns out at hsCRP of 0.8 isn't that low. According to Dr. Thomas Lewis, in his book "Uncovering Chronic Inflammation and Hidden Infections: The Untold Story Behind Chronic Disease Prevention and Reversal," the cutoff value is 0.6. I didn't pay much attention to it, but here's a research article that shows that supports the idea: HS-C Reactive Protein and Red Blood Cell Width as Effective Markers for Hypertension:

CRP won't necessarily be high with protein breakdown.
Studies with androgen deprivation shows that it increases muscle catabolism, leucine oxidation and urea production.
Is your androgens optimal?

 

[yerrag]

CRP won't necessarily be high with protein breakdown.
Studies with androgen deprivation shows that it increases muscle catabolism, leucine oxidation and urea production.
Is your androgens optimal?

I haven't taken any testosterone or DHEA-S tests yet. What other tests are needed?

So is there a possibility that my CRP would be lower if my androgens were optimal?

 

[Hans]

I haven't taken any testosterone or DHEA-S tests yet. What other tests are needed?

So is there a possibility that my CRP would be lower if my androgens were optimal?

I think DHEA-S and T would suffice for androgen test. DHT could also help, but that's expensive I've heard

Androgens can decrease CRP as they lower inflammation yes.

 

[yerrag]

Thanks. I'll check it out!

 

[khan]

Yeah I don't think you have to test it though.

Just to elaborate some more on the excess ATP consumption.

Shortage of Cellular ATP as a Cause of Diseases and Strategies to Enhance ATP
"During acute energy consumption, like extreme exercise, cells increase the favorability of the adenylate kinase reaction 2-ADP -> ATP+AMP by AMP deaminase degrading AMP to IMP, which further degrades to inosine and then to purines hypoxanthine -> xanthine -> urate. Thus, increased blood urate levels may act as a barometer of extreme energy consumption."

"decreased energy consumption from maintaining the pool of IMP for salvage to AMP and then ATP, since de novo IMP synthesis requires burning seven ATPs."

"If that purine salvage process fails to salvage Hx (hypoxanthine) back into high-energy phosphate molecules (AIP, AMP, ADP, ATP), and instead, XOR degrades it to X (xanthine), then X can only be further degraded by XOR to UA (uric acid)."

"after degradation to UA, new purine molecules would need to be salvaged from dietary intake or resynthesized de novo at an energy expense of 7 high-energy phosphate bonds from 6 ATP molecules to regenerate IMP"

"Previous results suggest that serum UA is a biomarker of ATP consumption, since rapid ATP consumption can lead to purine degradation and an increased rate of UA production in humans. For example, intense muscular exercise (Hellsten et al., 1999; Stathis et al., 1994, 1999), fructose challenge (Budillon et al., 1992; Donderski et al., 2015), alcohol intake (Lieber, 1965; Schmidt et al., 2013), and high brain activity (Salvadore et al., 2010; Goodman et al., 2016) can lead to energy crisis and resultant hyperuricemia. In addition, vascular regions undergoing ischemia-reperfusion may produce increased purine degradation products; a sign that a local energy crisis has occurred."
I would like to add that converting lactate back to glucose in the liver requires 6 ATP. Proteosomal degeneration also requires a lot of ATP and can elevate uric acid.

"Another study by the same group investigated the effect of angiotensin II (AII) on matrix metalloproteinase activity (MMP) in the canine heart. AII administration increased MMP activity, as well as chamber diastolic stiffening and MMP activity, and decreased tissue bioenergetics, while treatment with an MMP inhibitor was shown to decrease the effects of AII and reduce purine loss, likely through inhibition of AMPD activity (Paolocci et al., 2006)."

They found that the best way to increase ATP and lower uric acid was with a xanthine oxidoreductase (there are natural inhibitors) plus inosine.

What are the natural inhibitors of xanthine oxidoreductase?

 

[Hans]

What are the natural inhibitors of xanthine oxidoreductase?

Kaempferol, myricetin, quercetin, cinnamon essential oil, ellagic acid, phytic acid, caffeic acid, apigenin, epicatechin, propolis, etc, can be effective.

 

[Astolfo]

Yey :))))

@yerrag So yerrag, I was thinking that I have some sort of hypoxia problem rather than pssd. And I came across to this topic. So you say, metabolic problems --> increased lactate --> decreased uric acid excreation --> NO inactivation?

That's my recent blood test:

Ketogenic diet, dark chocolate has the most significant effect on my cognition. Now that makes sense. I have metabolic problems since pssd, I'm getting hungry much frequently and I gained significant belly fat. I think there is some sort of insuline resistance in my body. Also my pee is as clear as pure water since pssd.

Coffee makes me sleepier whenever I drink it and I guess it's because it antagonizes thiamin.

Brain Fog/sleepines After Coffee. Problems With Blood Flow/sulphur?

Coffee has thiamine antagonists blocking carbohydrate metabolism. I had to stop drinking coffee made me to tired. Pur caffeine and coke make no problem at all.

 

[Astolfo]

@yerrag how much b1 you would recommend?

 

[GorillaHead]

So inosine. xanthine oxidoreductase Inhibitors. Emodin?

anything else that best inhibits hypoxia?

 

[LLight]

Physiological functions and pathogenic potential of uric acid: A review - ScienceDirect

Spoiler: Uric acid function

Indeed, uric acid may exert fundamental roles in tissue healing via initiating the inflammatory process that is necessary for tissue repair, scavenging oxygen free radicals, and mobilizing progenitor endothelial cells [15].

https://www.researchgate.net/public...nt_status_following_osteosynthetic_operations

Spoiler: Xanthine oxidase function

The trace element levels of hospital patients whose bone fractures had received osteosynthetic treatment or had required the use of artificial replacement joints is reported. For molybdenum the immediately preoperative blood plasma level of Mo (0.7 microg/l) was below the normal level (1.20 microg/l) and decreased postoperatively (0.5 microg/l. This marked reduction of the Mo content of the blood plasma is attributed to a shift of Mo into the affected tissue, since the enzymes xanthine oxidase and sulfite oxidase, which require Mo as a cofactor, are essential enzymes of bone and connective tissue metabolism, functioning as part of a detoxification mechanism for accumulated cell debris. The extent of the reduction of the plasma Mo level could be a measure of the wound healing process. A deficiency of Mo due to increased demand from the wound could cause interference in the healing process.

 

[yerrag]

@yerrag So yerrag, I was thinking that I have some sort of hypoxia problem rather than pssd. And I came across to this topic. So you say, metabolic problems --> increased lactate --> decreased uric acid excreation --> NO inactivation?

I don't think I had that right. I think, and I may well be wrong, that decreased uric acid excretion (leading to high serum uric acid) reflects a need to retain anti-oxidants by the body to counteract chronic oxidative stress arising from inflammation.

So, in my case, I suspect immune complex deposits in my kidney nephrons cause an autoimmune reaction that is inflammatory. To counter the oxidative stresses involved, there is a high usage rate of anti-oxidants from the body's primary anti-oxidant system. If my albumin, which also serves a role as an antioxidant, isn't being used up so much, the body would not need to minimize uric acid excretion, seeing that there is no need for extra antioxidant capacity.

High serum uric acid, in my case, would signify high albumin usage, as indicated my low serum albumin and high albumin excretion in urine. The albumin being excreted may very well be oxidized albumin.