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Niacin - How to Beat the Flush

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In a previous articles I covered the tremendous health benefits of niacin supplementation, mediated via both lipid (cholesterol and blood fat) and non-lipid mechanisms, and what you need to know about niacin products:
Here I will explain what the notorious niacin flush is all about, and give you hands-on practical tips on how to beat it.

Niacin flush – what’s the fuss about?

Despite niacin’s tremendous health benefits, the infamous flushing has been a major impediment to the clinical use of niacin, and is the main reason for discontinuation of niacin supplementation.[1-3] Most people who start taking a niacin supplement will initially experience the flushing.[1-4] The niacin flush is not dangerous, but can be uncomfortable. The flush manifests as a “prickly heat” or a sense of warmth in the face, neck, ears, trunk, and, less frequently arms and legs.[5] This is often accompanied by itching, tingling and a reddening of the skin, usually in patches (known as erythema). 
Symptoms typically start 15-30 minutes after ingesting immediate-release niacin on empty stomach, and 30-120 minutes after ingesting extended-release niacin. Due to inconsistencies in time-release niacin products, their onset of flush occurs at more unpredictable and variable times.[2, 3] The exception is wax-matrix niacin, which is the most reliable time-release formulation.
The flush usually lasts for less than 1 hour to 2.5 hours.[2, 3] For somebody who has never taken a niacin supplement before, as little as 50 mg can result in the characteristic flush.[5] This is why doses should be escalated progressively. Taking an effective dose of 1000 mg (1g) the first time will cause very intense flush reaction over the whole body.[5]
The niacin flush is caused by the release of prostaglandin D2 (and possibly other eicosanoids) from cells in the skin.[6] It was recently demonstrated that niacin also activates the capsaicin receptor - which also mediates the heat sensation caused by consumption of spicy food - and that this activation of the capsaicin receptor contributes to the niacin flush.[7, 8]

Importance of informing people about the flush and how to deal with it

Flushing symptom severity is a strong predictor of niacin discontinuation.[9] One study reported that 27% of niacin users stopped taking niacin after 4 months, and those were the ones who were most bothered by the flush.[9] In contrast, discontinuation rates due to flushing in niacin studies are as low as 5%.[10] A study that specifically evaluate niacin compliance in a “real-world” primary care setting reported discontinuation due to flushing to be 10%.[11]
A shared characteristic among niacin studies reporting low discontinuation rates is the patient education procedures employed prior to study initiation.[10] This suggests that patient education may be a critical factor in niacin supplementation adherence. Support for this comes from a survey of patients in routine clinical practice who were prescribed niacin and reported a high rate of discontinuation; less than half of niacin users reported being advised by their physician to take aspirin to avoid flushing.[9] This underscores the importance of informing people about ways to mitigate the flush. 

How to beat the flush?

The onset and intensity of the flush is directly related to the niacin absorption rate and the consequent rate of elevation of blood niacin levels; once a constant blood niacin level is reached the flush starts to abate.[12] Therefore, fast niacin absorption, as seen with immediate-release niacin, causes a greater initial flush intensity than does extended-release niacin, which is absorbed slower.[13-15] However, even extended-release niacin may initially causes a flush reaction. The good news is that there are several ways to reduce the initial intensity of the flush:
Gradually increase daily niacin doses in a “start low go slow” manner and split up the daily dose
Immediate-release niacin should be administered in divided doses, after meals, and doses should be gradually increased.[16] A dose-escalation guideline is to start taking 50-100 mg twice daily for the first
week, then double the daily dose each week until the target dose is reached, ideally 1.5 to 3 g per day.[17] 750 mg taken 2-3 times per day for a total daily dose of 1,500 to 2,250 mg seems to work well for most people.
If you are using time-release niacin – make sure it is was-matrix niacin. I explained why you should chose the was-matrix version of time-release niacin in a previous article “Niacin Supplements - what you need to know about niacin products”. Start taking 250 mg 3 times per day, and build up the dose to 750 mg 2-3 times per day. Always take it after meals.
Extended-release niacin is recommended to be taken at bedtime, after the last daily meal.[18, 19] The prescribing information for extended-release niacin (known as Niaspan) suggests a starting dose of 500 mg for 4 weeks, which is increased in 500-mg increments every 4 weeks to 1 g (two 500-mg tablets) during weeks 5 to 8, 1.5 g (two 750-mg tablets) during weeks 9 to 12, and 2 g (two 1-g tablets) for the final 4 weeks.[20]
Take aspirin 30 min before taking niacin
Several studies shows that aspirin attenuates niacin flushing.[21-27] one study found that 325 mg of aspirin significantly attenuated flushing symptoms when administered 30 to 60 min, but not 15 or 120 min, before ingestion of 500 mg immediate-release niacin.[21] Notably, a higher aspirin dose of 650 mg was not better than 325 mg.[21] However, 325 mg of aspirin is superior to 80 mg in mitigating flushing with 500 mg of immediate-release niacin.[22] 325 mg of aspirin 30 min before niacin ingestion is also significantly superior to 200 mg of ibuprofen in blunting flushing and itching.[23] Taking 325 mg of aspirin 30 min before extended-release niacin (500 to 2000 mg) is also effective, and improves niacin adherence.[25] For greatest reduction in flush intensity, take aspiring before meals and niacin after meals.
Take niacin after meals
Take immediate-release niacin after meals, especially a high-fat meal, as that will slow down its absorption and thus reduce the flush intensity. 
Prescription extended-released niacin (Niaspan), which is ingested once daily, should be taken after the last daily meal. 
If you take any time-release niacin that is not wax-matrix – such as Slo-Niacin or Niaspan - is it best to take if some 40 min after meals. The reason is that the release mechanism of Slo-Niacin is degraded by peristaltic activity in the gut. Waiting a little bit after a meal will let the gut settle and allow for the time-release complex to work as it is supped to.
Develop tolerance to the flush
Most people don't know that continued niacin supplementation leads to development of tolerance to the flush.[28] This means that the intensity of the flush decreases or even completely vanishes with time, often within the first week or two, as long as niacin is taken regularly on a daily basis.[18, 19, 28, 29] Knowing this is critical, as most discontinuations take place during the first week of niacin supplementation, before tolerance has developed.[29] 
Flush tolerance is due in part to smaller increases of prostaglandin D2 production after long-term regular niacin ingestion.[28] However, if niacin supplementation is interrupted, one has to start from scratch and re-develop tolerance, as tolerance only exists as long niacin is taken. Hence, with niacin supplementation one has to stick to it!

Niacin sensitivity

Several studies have shown that many of the people who appear to be intolerant of niacin, primarily because of the flush, are often just more sensitive to niacin and do well on a reduced dose.[30-32] It appears likely that much of what has been presumed to be niacin intolerance may simply be overdosing of niacin in sensitive individuals.[32] 
The possibility that some people may have higher niacin sensitivity was demonstrated in an 11 month study with a dose reduction protocol, where niacin sensitive subjects who completed the study on less than 1000 mg/day actually had comparable lipid results to subjects on the full dose of 2000 mg/d.[30] Another study found that taking 435 mg immediate-release niacin per day for 1 year elevates HDL levels by 20% while reducing triglyceride levels by 9%.[33] One study showed that an even lower dose of niacin (50 mg twice daily) increased HDL by 6% in statin treated patients.[34]
Thus, if you cannot tolerate a full dose of immediate-release niacin or time-release niacin, don’t fret. You may still derive substantial health benefits with a lower dose. 



BOX: Practical advice on how to take niacin supplements
With immediate-release niacin, start taking 100 mg twice daily for the first week, then double the daily dose each week until the target dose is reached, ideally 1500 to 3000 mg per day.
With time-release niacin – ideally wax-matrix niacin – start taking 250 mg 3 times per day, and build up the dose to 750 mg 2-3 times per day.
Spread out intake over the day and take some 40 min after meals to dampen the niacin flush. 
If the flush makes you uncomfortable, taking 325 mg aspirin about 30 minutes prior to niacin reduces the flushing intensity. Try taking the aspiring before meals, and then the niacin after meals.
Stick to it! With regular daily niacin supplementation, tolerance develops to the flush. Over time, the flush sensation can disappear completely in people who diligently keep taking niacin every day.






Niacin – a.ka. vitamin B3 - is a unique broad spectrum cholesterol “drug”. The reason it has not been getting the attention it deserves in the medical community and among health conscious people, is the flush.
While the niacin flush may be uncomfortable, it is not dangerous; it is a natural reaction to high-dose niacin. As outlined here, there are several simple ways to mitigate this flush. This will help you stick with the niacin supplementation and develop tolerance to the flush, and ultimately reap its wide array of health benefits.
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1.            Kei, A., E.N. Liberopoulos, and M.S. Elisaf, What restricts the clinical use of nicotinic acid? Curr Vasc Pharmacol, 2011. 9(4): p. 521-30.

2.            Guyton, J.R. and P.D. Simmons, Flushing and other dermatologic adverse events associated with extended-release niacin therapy. J Clin Lipidol, 2009. 3(2): p. 101-8.

3.            Davidson, M.H., Niacin use and cutaneous flushing: mechanisms and strategies for prevention. Am J Cardiol, 2008. 101(8A): p. 14B-19B.

4.            Kamanna, V.S., S.H. Ganji, and M.L. Kashyap, The mechanism and mitigation of niacin-induced flushing. Int J Clin Pract, 2009. 63(9): p. 1369-77.

5.            Carlson, L.A., Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review. J Intern Med, 2005. 258(2): p. 94-114.

6.            Morrow, J.D., et al., Identification of skin as a major site of prostaglandin D2 release following oral administration of niacin in humans. J Invest Dermatol, 1992. 98(5): p. 812-5.

7.            Clifton, H.L., et al., TRPV1 channels are involved in niacin-induced cutaneous vasodilation in mice. J Cardiovasc Pharmacol, 2015. 65(2): p. 184-91.

8.            Ma, L., et al., Nicotinic acid activates the capsaicin receptor TRPV1: Potential mechanism for cutaneous flushing. Arterioscler Thromb Vasc Biol, 2014. 34(6): p. 1272-80.

9.            Kamal-Bahl, S., D.J. Watson, and B.M. Ambegaonkar, Patients' experiences of niacin-induced flushing in clinical practice: a structured telephone interview. Clin Ther, 2009. 31(1): p. 130-40.

10.          Brinton, E.A., et al., Niacin extended-release therapy in phase III clinical trials is associated with relatively low rates of drug discontinuation due to flushing and treatment-related adverse events: a pooled analysis. Am J Cardiovasc Drugs, 2011. 11(3): p. 179-87.

11.          Vogt, A., et al., Evaluation of the safety and tolerability of prolonged-release nicotinic acid in a usual care setting: the NAUTILUS study. Curr Med Res Opin, 2006. 22(2): p. 417-25.

12.          Svedmyr, N., L. Harthon, and L. Lundholm, The relationship between the plasma concentration of free nicotinic acid and some of its pharmacologic effects in man. Clin Pharmacol Ther, 1969. 10(4): p. 559-70.

13.          Pieper, J.A., Understanding niacin formulations. Am J Manag Care, 2002. 8(12 Suppl): p. S308-14.

14.          Piepho, R.W., The pharmacokinetics and pharmacodynamics of agents proven to raise high-density lipoprotein cholesterol. Am J Cardiol, 2000. 86(12A): p. 35L-40L.

15.          McKenney, J., New perspectives on the use of niacin in the treatment of lipid disorders. Arch Intern Med, 2004. 164(7): p. 697-705.

16.          Brown, W.V., et al., The use of niacin. J Clin Lipidol, 2009. 3(2): p. 65-9.

17.          ASHP Therapeutic Position Statement on the safe use of niacin in the management of dyslipidemias. American Society of Health-System Pharmacists. Am J Health Syst Pharm, 1997. 54(24): p. 2815-9.

18.          Capuzzi, D.M., et al., Efficacy and safety of an extended-release niacin (Niaspan): a long-term study. Am J Cardiol, 1998. 82(12A): p. 74U-81U; discussion 85U-86U.

19.          Guyton, J.R., et al., Effectiveness of once-nightly dosing of extended-release niacin alone and in combination for hypercholesterolemia. Am J Cardiol, 1998. 82(6): p. 737-43.

20.          Abbott Laboratories NIASPAN™ (niacin extended-release tablets) US prescribing information. Available at: http://www.niaspan.com2005.

21.          Jungnickel, P.W., et al., Effect of two aspirin pretreatment regimens on niacin-induced cutaneous reactions. J Gen Intern Med, 1997. 12(10): p. 591-6.

22.          Whelan, A.M., et al., The effect of aspirin on niacin-induced cutaneous reactions. J Fam Pract, 1992. 34(2): p. 165-8.

23.          Dunn, R.T., et al., Low-Dose Aspirin and Ibuprofen Reduce the Cutaneous Reactions Following Niacin Administration. Am J Ther, 1995. 2(7): p. 478-480.

24.          Cefali, E.A., et al., Aspirin reduces cutaneous flushing after administration of an optimized extended-release niacin formulation. Int J Clin Pharmacol Ther, 2007. 45(2): p. 78-88.

25.          Thakkar, R.B., et al., Acetylsalicylic acid reduces niacin extended-release-induced flushing in patients with dyslipidemia. Am J Cardiovasc Drugs, 2009. 9(2): p. 69-79.

26.          Alves, J.D., et al., Influence of the timing of low-dose aspirin on tolerability of prolonged-release nicotinic acid in patients at elevated cardiovascular risk. Curr Med Res Opin, 2008. 24(10): p. 2815-20.

27.          Oberwittler, H. and M. Baccara-Dinet, Clinical evidence for use of acetyl salicylic acid in control of flushing related to nicotinic acid treatment. Int J Clin Pract, 2006. 60(6): p. 707-15.

28.          Stern, R.H., et al., Tolerance to nicotinic acid flushing. Clin Pharmacol Ther, 1991. 50(1): p. 66-70.

29.          Paolini, J.F., et al., Measuring flushing symptoms with extended-release niacin using the flushing symptom questionnaire: results from a randomised placebo-controlled clinical trial. Int J Clin Pract, 2008. 62(6): p. 896-904.

30.          Alderman, J.D., et al., Effect of a modified, well-tolerated niacin regimen on serum total cholesterol, high density lipoprotein cholesterol and the cholesterol to high density lipoprotein ratio. Am J Cardiol, 1989. 64(12): p. 725-9.

31.          Keenan, J.M., et al., Niacin revisited. A randomized, controlled trial of wax-matrix sustained-release niacin in hypercholesterolemia. Arch Intern Med, 1991. 151(7): p. 1424-32.

32.          Keenan, J.M., Wax-matrix extended-release niacin vs inositol hexanicotinate: a comparison of wax-matrix, extended-release niacin to inositol hexanicotinate "no-flush" niacin in persons with mild to moderate dyslipidemia. J Clin Lipidol, 2013. 7(1): p. 14-23.

33.          Luria, M.H. and D. Sapoznikov, Raising HDL cholesterol with low-dose nicotinic acid and bezafibrate: preliminary experience. Postgrad Med J, 1993. 69(810): p. 296-9.

34.          Wink, J., G. Giacoppe, and J. King, Effect of very-low-dose niacin on high-density lipoprotein in patients undergoing long-term statin therapy. Am Heart J, 2002. 143(3): p. 514-8.

Last modified on Wednesday, 04 April 2018 18:34

Medical Writer & Nutritionist

MSc Nutrition

University of Stockholm & Karolinska Institute, Sweden 

   Baylor University, TX, USA

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