I drink about 500mg coffee in the morning and usually take a nicotine zyn about 4 pm. Would this play a part in higher BP.
Absolutely will cause heightened blood pressure.I drink about 500mg coffee in the morning and usually take a nicotine zyn about 4 pm. Would this play a part in higher BP.
The blood pressure should go down as you ease on the caffeine. If you take citrulline/arginine daily, that can help as well. As long as you are on caffeine, you will have heightened BP. The more caffeine, the heightened you BP may be.What do you recommend in terms of caffeine daily? How long will this cause increased blood pressure ? Will try and cut in half for a week and see. Hoping see results
It's going to depend on if you can cut back on the caffeine a lot, or even drop it all together. You may drop caffeine in half and have higher BP than normal. It may take dropping it all together to get it in a range where you would like it, and yes, even after dropping the caffeine, it could take a few days to get your BP where you desire it.Guess 3-4 days possibly?
I’d wager It’s the nicotine... not the caffeine. 18mg in a single dose- is quite a bit.Yeah. I am done with espresso shots. That’s my main issue I think. Just going to try 300mg day for a week and see what happens. Hoping to flush excess caffeine out from past. How long would you think to see if lowering to 300mg works ok ?
winner...i have a friend who recently quit smoking and even using a 4mg lozenge raised his bp...he was using 6 daily and once he started cutting back his bp started dropping...now that he is off completely his bp is lower than it was originally when he was a smoker.I’d wager It’s the nicotine... not the caffeine. 18mg in a single dose- is quite a bit.
Can you show any evidence of that first point re nicotine?Nicotine independently of cigarette smoking causes atherosclerosis which leads to hypertension.
Secondly, do you consume 500mg of COFFEE (ie. 2.25 cups) or do you consume 500mg of CAFFEINE. Thats a very important distinction as the latter would only yield 215mg (when using an avg of 95mg/cup) and thats not really a ton whatsoever. (Edit: nvm, i didnt see there was a second page - 500mg in one dose is a lot lol).
But, if she used too small of a cuff that could artificially inflate your reading. Or you could just have white coat htn. You need multiple elevated readings to really be diagnosed with true htn.
The #s above the first article are for the article headings the quotes are from so you can find the statements easier.Can you show any evidence of that first point re nicotine?
Thanks.The #s above the first article are for the article headings the quotes are from so you can find the statements easier.
#1 - 2013
1. Pathogenesis of tobacco-related vascular disease
“In addition to its role as the habituating agent in tobacco, nicotine also accelerates vascular disease.”
“In addition to these actions mediated by activation of the sympathetic nervous system, nicotine has direct actions on the cellular elements participating in plaque formation.”
2. Pathological neovascularization and the endothelial nAChR
“Of relevance to the current paper, nicotine increases plaque progression and neovascularization in the ApoE−/− mouse (8). This effect of nicotine was independent of plasma lipid values and was blocked by rofecoxib, a known inhibitor of angiogenesis.”
3. Exploring the role of the nAChR in atherosclerosis
“On Oct 27 2010, the FDA held a public workshop to discuss the risks and benefits of approving long-term use of NRT (ie. beyond the current approved maximum period of 12 weeks). This workshop revealed that, whereas short-term use of NRTs has been shown to be safe and effective in tobacco cessation, there are little clinical data on the safety and efficacy of long-term use of NRTs. Taken together with other pre-clinical research, the current study suggests that nicotine itself may accelerate atherosclerotic disease. Until clinical data are available on long-term use of nicotine, the astute clinician may wish to substitute other approaches toward tobacco cessation if short-term use of nicotine fails.”
Additionally, theres other info on cellular mechanisms regarding alpha-1 and “muscle type” nAChRs described in the paper as well.
The role of nicotine in the pathogenesis of atherosclerosis
www.ncbi.nlm.nih.gov
#2 - 1992
“Smoking or long-term nicotine administration has been shown to cause endothelial injury, as indicated by the increase in the number of circulating endothelial cells13-16 and the increase in endothelial permeabili- ty,1718 as well as the morphological changes of the endothelium.18"23 Repeated endothelial damage has been suggested as an initiating factor in the pathogenesis of atherosclerosis
24, 25.”
“As shown in Table 1, the frequency of endothe- lial cell death was significantly higher (0.94±0.11% versus 0.40±0.04%, p/?kg) rats than in control rats.”
Then just read the entire discussion from the AHA article below. Some of it is claims made about “cigarette smoking” but at other points they make statements about nicotine. Including one part that states nicotine has been shown to cause not only endothelial cell death, but also reduced endothelial cell mitosis (which, we can assume, would help replenish/replace those dead cells).
#3 - 2018
For the next study, published in Nature, im not going to go through it as much but ill include 2 short excerpts:
“Increasing evidence has demonstrated that nicotine impairs the cardiovascular system by targeting vascular endothelial cells, but the underlying mechanisms remain obscure. It is known that cell death and inflammation are crucial processes leading to atherosclerosis. We proposed that pyroptosis may be implicated in nicotine-induced atherosclerosis and therefore conducted the present study.”
“Substantial evidence supports the promoting effect of nicotine on atherosclerosis in a long-term basis5, even though short term exposure to nicotine is considered relatively harmless.”
Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis - Cell Death & Disease
Cigarette smoking is a major risk factor for atherosclerosis and other cardiovascular diseases. Increasing evidence has demonstrated that nicotine impairs the cardiovascular system by targeting vascular endothelial cells, but the underlying mechanisms remain obscure. It is known that cell death...www.nature.com
The first study I posted would support your interpretation that nicotine “may” promote or accelerate atherosclerosis, but it seems that the overall balance would lean more towards it being atherogenic than it being non-atherogenic and especially protective. I also agree with you that animal data doesnt always carry over to humans, but it doesnt change the fact that nicotine has been repetitively shown to be atherogenic in both mice and rabbits. Those results shown over and over again combination with the fact we know how atherogenic tobacco smoking is leads me to believe it very likely does have at least one, if not multiple, atherogenic mechanisms.Thanks.
I think the balance of findings suggest nicotine “may” accelerate development of atherosclerosis in mice bred to be susceptible the disease. Research is far from proving a causative effect in humans however.
For instance, the agonism of α7nAChR has been show to prevent atherosclerosis in this study:
https://www.sciencedirect.com/science/article/abs/pii/S0021915019313711
I think distinguishing between a healthy and diseased population is an important distinction in this case. As well as method of delivery, dosage, exposure length and genetic polymorphisms.
No not diseased per se, but Apoe-/- mice are specifically genetically prone to developing atherosclerosis, was the point I was trying to make.The first study I posted would support your interpretation that nicotine “may” promote or accelerate atherosclerosis, but it seems that the overall balance would lean more towards it being atherogenic than it being non-atherogenic and especially protective. I also agree with you that animal data doesnt always carry over to humans, but it doesnt change the fact that nicotine has been repetitively shown to be atherogenic in both mice and rabbits. Those results shown over and over again combination with the fact we know how atherogenic tobacco smoking is leads me to believe it very likely does have at least one, if not multiple, atherogenic mechanisms.
I also dont necessarily agree that every study done on the topic was in diseases subjects, or that nicotine wouldnt still cause atherosclerotic changes in healthy individuals. From what I saw (or at least that I recall from seeing) in those studies above, i dont think any of the animals were previously diseased.
I also completely agree that dosage and duration likely play a huge role - as was noted multiple times in at least one of those studies above where they stated nicotine replacement therapy to aid with cigarette smoking cessation is completely safe in the short term.
Gotcha, understood. Thanks for that clarification.No not diseased per se, but Apoe-/- mice are specifically genetically prone to developing atherosclerosis, was the point I was trying to make.
May be beneficial to get caffeine powder and try to reduce it that way. Start pulling back slowly (25-50mg weekly unless you’re wanting to taper quicker).Yes. Lately at night I’ve been taking it and it’s 126 over 76. Heart rate resting is under 60. I believe my heart is great, just have to cut down on caffeine. A hard thing to do
Yeah, I missed the nighttime 126/76. That isn't something to really stress about, IMO. Try taking it when you first wake up in the morning as well. Get some readings at different times and you may figure out some things.511 200. Ab 13-14% bf. Real lean for almost 40. Workout and cardio for years. Never miss. I think it’s nicotine. Everything I read leads back to this. Going to quit for a week and see if it naturally lowers. If not going to doctor. My heart has been tested and always comes back great. I stopped chewing tabocco a few years ago but started nicotine pouches which I think it was nicotine in chewing tabocco causing high bp than normal
Give it 7 days. Nicotine has a shorter half life and should be damn near completely cleared by now but it’s primary metabolite can take 5+ days to clear (based on the 5x half life typically used to estimate when a drug will be “out of the system”). I also dont know a ton about cotitine other than it’s being studied for some psychiatric conditions, so i dont really know if it has the same potential hypertensive effects as the parent compound nicotine. Like you said, could also be rebound from withdrawal. Either way, just give it 7 days.3 days no nicotine and pressure seems worse at night. It usually hits me about 1 pm or so. Only drink 200-300mg caffeine. Maybe it’s withdraw symptoms? Hopefully next week it’s better or else I need to figure something out. T
I mean...are you drinking the caffeine within an hour of your bp elevating? If so then yah it could absolutely be contributing and very likely is if theres that close of a temporal relationship between dosing & bp elevation. If youre drinking it 3+ hrs before and it doesnt get elevated til 1pm id have a hard time blaming the caffeine.I mean no way 200-300mg caffeine should cause consistently all the time high bp?
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