I have low MAO-A activity that results in the slow breakdown of neurotransmitters but more importantly in my case amines such as Tyramine and histamine which leads to frequent adverse reactions (hypertensive crisis, heart palpitations) to eating certain foods.
I’m interested to know if there are any treatments, medications or supplements that can increase the activity of MAO-A?
I’ve read vitamin B2 (riboflavin), progesterone and white mulberry have shown some promise but I’m interested to learn of others experiences.
So for a practical course in my master's program I isolated an unknown strain from a nearby river and after 16s sequencing it was a 92.95% match with Acinobacter johnsonii. However, literature shows that this strain should be oxidase negative, but our strain was oxidase positive. I am trying to find out what could explain this discrepancy. My thinking so far is that A. johnsonii is naturally competent so maybe our strain took up some DNA that conferred cytochrome oxidase. Does anyone know if that is a reasonable explanation? Also I want to compare the characteristics of A. johnsonii with some of the other characteristics we identified in our strain (nitrogenase positive for example) does anyone have a good resource for looking at the physiological characteristics of diffrent bacteria? Thanks for any and all help!
I have been dealing with Dyshidrosis for 20 years and have been unable to find my trigger. I generally have sweaty hands so I figured that was the cause.
Recently, I ran out of my daily antihistamine (Zyrtec) and, because of supply chain issues, was out for 3 days. This resulted in the worst Dyshidrosis episode I have ever had. Unclear if this was the cause or not, but it got me thinking.
After some research, I realize that some people have histamine intolerance and that can result in eczema. I also see that some people change their diets and take supplements like DAO to help deal with histamines in food.
Anyone with experience with these supplements? I’m sick of the same routine of seeing my dermatologist and getting steroid creme as a result… so willing to try something new.
Disclaimer: I am not a medical professional and this is not medical advice. Follow at your own discretion.
Histamine intolerance (HIT) is thought to be caused by a disproportionate amount of histamine in the body. The enzyme diamine oxidase (DAO) is considered for the gastrointestinal degradation of histamine. For this open-label interventional pilot study, we identified 28 patients with HIT. For 4 weeks, they were instructed to take DAO capsules before meals. Then, throughout a follow-up period, they were instructed not to take the DAO. We used a questionnaire that included 22 symptoms, which were divided into 4 categories, as well as a symptom severity score. All symptoms improved significantly during the oral supplementation of DAO. During the follow-up period, without DAO supplementation, the symptoms sum scores increased again. The symptom intensity score was reduced for all symptoms. We have demonstrated, a significant reduction of every HIT-related symptom and its intensity due to DAO oral supplements.
The symptoms of the skin—pruritus, urticaria, flush and swollen, reddened eyelids—significantly improved with DAO ingestion (Dunn p < 0.01; Wilcoxon p = 0.001).
https://link.springer.com/article/10.1007/s10068-019-00627-3
Tldr: You're low on diamine oxidase enzymes. You could try DAO supplements with each meal.
Questions to further look into
- Why are you low on DAO?
- What made you low on DAO?
- How can you you increase DAO?
I read that DAO supplements can help or cure your CU. Has anybody experience with DAO supplements? I have CU since 9 years in winter. Now i am on xolair since 10 days, i wait for the second injection. But i am still interested to find a solution for this condition..
Greetings
Regulation of lipids is central to replicative senescence - Molecular BioSystems (RSC Publishing)
Free fatty acids, insulin resistance, and type 2 diabetes mellitus - PubMed (nih.gov)
With a layman's understanding of physiology, I have found it convincing that the BCL-xl inhibitors will allow for the release of cytochrome oxidases from the mitochondria which causes targetted apoptosis.
Free Fatty Acids naturally cause an inhibition of cytochrome oxidases and block cytochrome oxidase-reliant respiration. Elevated FFAs are also central to Diabetes and metabolic syndrome. There are few metabolites which are not able to be disposed of by the body. However, the unstable Poly-unsaturated fats in certain conditions produce metabolites such as lipofuscin which have only one pathway but to be stored in soft tissue. Some of these metabolites are stored in cells and accumulate with age leading to senescent activity (see first article above.) Diabetes makes this process much worse (see second article.)
Essentially, UBX1325 is dealing with this issue, exacerbated by diabetes, which causes cells to be suspended in a low-functional, anti-apoptosis state. There is no fixing these cells and there is no ability for the body to regulate them because they pathologically block the cytochrome oxidase activity required to remove them. Because UBX1325 inhibits BCL-xl it restores this cytochrome oxidase activity to help the body do what it does naturally.
UBX is on to something.
tl;dr Diabetes is associated with elevated free fatty acids, free fatty acids are responsible for senescence by blocking cytochrome oxidase and protected through BCL-xl. UBX1325 blocks BCL-xl to let the body destroy these cells damaged by FFAs, through cytochrome oxidase pathway of apoptosis.
They both catalyze the oxidation of aldehydes into carboxylic acids, so what's the difference between them?
I have tried Riboflavin and it has had desired effects but I feel out of control / impulsive for next day or two. I have tried the dose of 100 mg.
What else is out there?
I've been having trouble with side effects from both allopurinol and febuxostat, so I did a little research on what other drugs are under development or already on the market. One in particular that caught my eye is topiroxostat (brand names: Topiloric, Uriadec).
From ScienceDirect:
>A novel, nonpurine, selective xanthine-oxidase inhibitor, topiroxostat bears dual inhibitory effects that combine the mechanisms of action of its predecessors. Similar to febuxostat, topiroxostat reduces uric acid production through chemical structure-based inhibition of xanthine oxidase. Akin to allopurinol, the drug covalently binds to, and inhibits, molybdenum-pterin, the active center of xanthine oxidase. Currently approved in Japan at doses ranging from 20 to 80 mg twice daily, topiroxostat 120 mg/day has been shown to be equivalent to allopurinol 200 mg in meeting serum urate target levels.17 Although the half-life of topiroxostat is reported to be 20 h, the agent may have additional, more persistent effects: studies suggest that once inhibited by topiroxostat, xanthine oxidase enzyme function never fully recovers even after disassociation of the drug-enzyme complex.18
>
>A 22-week randomized controlled trial analyzed the efficacy of topiroxostat versus placebo in patients with stage 3 chronic kidney disease. 90% of patients receiving topiroxostat (160 mg/day) achieved an serum urate (SU) target level of <6.0 mg/dL. Additionally, the percent decrease of SU in the topiroxostat group was 45.38%, compared with 0.08% in the placebo group. No serious adverse effects of topiroxostat were recognized when compared with placebo, but increases in liver enzyme elevations were more common in the intervention group.19
It does not appear that this is available in the U.S., and it's not clear to me that it's even widely used in Japan. It caught my eye nonetheless because it's apparently the only xanthine-oxidase inhibitor other than allopurinol and febuxostat that made it onto the market.
I would be very curious to know whether my body tolerates topiroxostat any better than it does allopurinol and febuxostat, but I guess I will never find out since it doesn't seem to be available here.
Does anyone else know anything about this drug, or others that are under development?
The purpose of this study was to explore the hypouricemic effect in hyperuricemia mice of triterpenoid acids from Inonotus obliquus (TAIO), and decipher of the underlying xanthine oxidase inhibitory mechanism. Measurement of xanthine oxidase (XO) inhibitory activity was assayed. Organ indexes and serum biochemical indicators were measured in potassium oxonate-induced hyperuricemia mice.
Studies showed that TAIO had the strong inhibitory effect on XO activity, and its inhibition type was mixed and reversible. In vivo, TAIO decreased efficiently uric acid level, hepatic XO, serum blood urea nitrogen activities in hyperuricemia mice. Indicating that TAIO may ameliorate kidney damage and relieve inflammation in hyperuricemic mice, and had the inhibitory effect on XO activity. Furthermore, eight triterpenoids were identified by Ultra performance liquid chromatography electrospray quadrupole time of flight mass spectrometry.
These findings proved that triterpenoids from Inonotus obliquus would have potential biological characteristics and effect on controlling hyperuricemia and gout as an active supplement.
From :
- https://onlinelibrary.wiley.com/doi/abs/10.1111/jfbc.13932
It happened to me.I only got one bottle parnate.I'm running out of medicine.I can't buy medicine at a Canadian pharmacy without a prescription
