Does Cold Weather Thicken Your Blood?
Does cold weather thicken your blood? Measurably, yes — and it does not take a blizzard. In the clearest experiment on the question, healthy volunteers who spent six hours in a 75 °F room with a fan blowing finished with whole-blood viscosity 21 percent higher than their blanketed partners, without their core temperature falling more than 0.4 °C. The change is not more blood cells; it is water leaving the plasma. This article covers what that study and the ones that followed it found, why fibrinogen runs higher in winter, why the cold switches off your thirst at the moment it matters, what the evidence says helps, and where daily support for healthy blood viscosity and circulation from a nattokinase supplement fits.
In this article: What a cool room did to eight volunteers · Where the fluid goes: plasma, not red cells · Colder blood is thicker blood, too · Why fibrinogen is higher in winter — and the two explanations · The thirst switch turns off in the cold · What the evidence supports · Where Great Billiom Nattokinase 10,800 FU fits
What a cool room did to eight volunteers
The experiment that answers the question was published in the BMJ in 1984 by Keatinge and colleagues. Eight healthy, unmedicated volunteers — four men and four women, aged 18 to 25 — were studied in pairs. One of each pair lay on a net bed for six hours in moving air at about 10 meters per second (roughly 22 mph) at 24 ± 1 °C, which is 75 °F, wearing a short-sleeved cotton shirt and shorts. The partner "lay on a couch for the same time with the same clothing but with two blankets and in still air." Forty-eight hours later they swapped roles.
The cooled volunteers' core temperature fell only 0.4 °C. Their blood changed anyway. Packed cell volume — the share of blood made up of red cells — rose about 7 percent, while red cell volume itself "did not change significantly," which means plasma had left the bloodstream rather than cells being added to it. The platelet count rose by 23 × 10⁹ per liter against 7 in the controls. "Whole blood viscosity increased by 21%; plasma viscosity usually increased, and arterial pressure rose on average from 126/69 to 138/87 mm Hg." The timing is worth noting: "Little of these increases occurred in the first hour." The first hour in the cold felt like the next five; the blood had not yet caught up.
The authors' interest was a public-health question about winter mortality; this article stays with the physiology they measured, which is the part that applies to anyone who has sat through a cold afternoon at a football game or in an under-heated office.
Where the fluid goes: plasma, not red cells
If the cells do not multiply, the plasma must shrink, and a second experiment from the same laboratory measured by how much. In Clinical Science in 1994, Neild and colleagues cooled six elderly (66–71) and six young (20–23) volunteers for two hours in moving air at 18 °C, or 64 °F. Trunk skin temperature fell from 35.5 to 29.5 °C "with little change in core temperature." The red cell count rose from 4.29 to 4.69 × 10¹² per liter without any change in cell size, "indicating a 14% or 438 ml decline in plasma volume" — by our arithmetic, close to two US cups of water gone from the circulation in two hours.
Where did it go? Only part of it out of the body. The volunteers excreted more water, sodium and potassium in the cold, but that "accounted for loss of only 179 ml of extracellular water." The rest had moved out of the vessels into the tissue fluid between cells. Plasma fibrinogen rose with the concentration — from 2.97 to 3.39 g/l in the older group and from 1.84 to 2.07 g/l in the younger — and the increases were "close to those expected from the fall in plasma volume." The body was not making more fibrinogen in two hours; it was carrying the same amount in less water.
The urine half of that story has a name, cold-induced diuresis, and a 2015 review in Sports Medicine by Sawka, Cheuvront and Kenefick explains why it matters more than sweating does for the blood specifically. Cold "stimulate[s] diuresis with solute losses, thus inducing an isotonic hypovolemia," and that kind of water loss "results in greater plasma loss for a given water deficit than hypertonic hypovolemia from sweat loss." Sweat pulls water from the whole body; the cold pulls it preferentially from the plasma.
Colder blood is thicker blood, too
Concentration is one mechanism. Temperature itself is another, because blood, like honey, flows more slowly when it is cooler. A 2001 study in the American Journal of Hypertension measured blood from 53 healthy adults in a capillary viscometer at three temperatures. "When temperature decreased from 36.5 degrees C to 22 degrees C, blood viscosity increased 26.13%," red cells became 34.73 percent less deformable, and plasma viscosity rose 18.71 percent; across all the readings, temperature and viscosity tracked each other closely (r = −0.84). Warming the same blood to 39.5 °C cut viscosity by 10.38 percent.
That 22 °C figure is a bench temperature, not a body temperature; your core sits near 37 °C whatever the forecast says. But blood passing through skin that has cooled to 29.5 °C, as the trunk did in the 18 °C experiment above, is not at 36.5 °C either, and fingers get colder still. This is the blood-side half of the story we told in our article on cold hands and feet: the body narrows the vessels in the hands and feet to protect the core, and the blood that does reach them is cooler and, at that temperature, thicker.
Why fibrinogen is higher in winter — and the two explanations
The two-hour experiments show concentration. A season shows something else. In a 1991 Lancet study, Stout and Crawford visited 100 people aged 75 and over every month for a year, recording body and room temperatures and drawing blood. Fibrinogen, plasma viscosity and HDL cholesterol all moved with the seasons, and "plasma fibrinogen concentrations showed the greatest seasonal change and were 23% higher in the coldest six months compared with summer months." Fibrinogen moved against the thermometer — it was "negatively related to core body temperature and all measures of environmental temperature."
Three years later a second Lancet study by Woodhouse and colleagues followed 96 people aged 65 to 74 through a year and found the same direction with a different cause. Fibrinogen was 0.13 g/L higher in winter (95% CI 0.05–0.20), but once season was accounted for it was "strongly related to neutrophil count," C-reactive protein, "self-reported cough" and "coryza" — a head cold — "but not to ambient temperature." Their explanation: winter respiratory infections raise fibrinogen through the body's acute-phase response, the same inflammatory surge that makes you feel wretched for three days in January.
Both can be true. Cold concentrates the fibrinogen you already have; a cold makes more of it. Either way, the protein that rises is the precursor of fibrin, and if that chain is new to you, our explainer on what fibrin is covers how fibrinogen becomes fibrin and how the body takes it apart again every day.
The thirst switch turns off in the cold
Here is the mechanism that lets winter dehydration sneak up on you. In Medicine & Science in Sports & Exercise, Kenefick and colleagues had men stand and walk in 4 °C (39 °F) and 27 °C (81 °F) air, both well hydrated and short of water. "When either euhydrated or hypohydrated, cold exposure attenuated thirst by up to 40% at rest and during moderate-intensity exercise." The water-conserving hormone vasopressin fell in the cold even when plasma osmolality — the signal that should raise it — was elevated.
The authors' explanation ties the whole picture together: narrowed vessels in the skin push blood toward the core, the core's volume sensors read "plenty," and the brain stands down both thirst and water conservation. So the cold moves water out of your plasma, sends part of it to the bathroom, and then tells you that you are not thirsty. People who drink to thirst in winter are drinking to a gauge that reads low.
What the evidence supports
What the evidence supports | What was found | Source |
Warm the trunk before the fingers | A shirt and shorts in a 75 °F breeze were enough to concentrate the blood; trunk skin fell 6 °C in 64 °F moving air | Keatinge 1984; Neild 1994 |
Cut the wind | The 24 °C experiment needed moving air at about 10 m/s to work; still air with two blankets was the control that did not change | Keatinge 1984 |
Count the hours, not the first one | "Little of these increases occurred in the first hour"; two hours at 18 °C removed 14 percent of plasma volume | Keatinge 1984; Neild 1994 |
Drink on a schedule, not on thirst | Cold cut thirst by up to 40 percent while plasma osmolality was elevated | Kenefick 2004 |
Expect to urinate more, and replace it | Cold drives a diuresis that takes more plasma per milliliter lost than sweating does | Sawka 2015 |
Count a head cold as a fibrinogen event | Winter fibrinogen tracked cough, coryza and inflammatory markers, not the thermometer | Woodhouse 1994 |
Two of these rows connect to things this blog has covered. The trunk-first row is the same lesson the cold-hands research teaches from the skin side: the hypothalamus decides how much blood the hands get based on whole-body warmth, so a layer on the torso does more than a thicker glove. And none of the cooling experiments had their volunteers move — Keatinge's lay on a net bed for six hours — which is the opposite of what our review of what 24 trials show about circulation while sitting found protects leg blood flow: two to three minutes of leg movement every 20 to 30 minutes. A cold stadium seat combines both.
When is any of this a doctor question? The experiments above describe healthy adults whose blood returned to baseline once they warmed up. Fingers or toes that change color in the cold, pain that does not fade on rewarming, or cold hands that arrive with other symptoms are the thresholds we set out in the cold-hands article, and they belong to a clinician, not a blog.
Where Great Billiom Nattokinase 10,800 FU fits
Warmth, wind protection and water on a schedule are what the cold research points to, and they work this afternoon. Nattokinase belongs to a longer time frame. It is an enzyme from natto, the fermented soybean dish, whose research is about supporting healthy blood flow and circulation over months rather than across one cold day. No nattokinase trial has measured blood viscosity or fibrinogen after cold exposure, or compared winter with summer, so this article makes no claim about a cold room on the enzyme's behalf. What the formula is built for is daily circulation support, and Great Billiom positions it exactly there: healthy blood flow, healthy blood viscosity and healthy fibrin metabolism, with "cold hands" named on the product page as one of the everyday signs that your circulation deserves more attention.
Great Billiom Nattokinase delivers 10,800 FU per two-capsule serving. That matches the higher dose arm of the largest nattokinase study to date, 1,062 adults followed for 12 months in Frontiers in Cardiovascular Medicine, whose authors note plainly that it "represents a retrospective study and not a randomized control trial." Each serving also carries 180 mcg of vitamin K2 (MK-7) and 240,000 SPU of serrapeptase in delayed-release vegetarian capsules — 90 capsules, 45 servings, $19.99, or $17.99 on Subscribe & Save. The label directs two capsules daily on an empty stomach, at least an hour before or two hours after a meal; many people take theirs before bed. Nattokinase contains soy. Anyone taking an anticoagulant, antiplatelet or blood-pressure medication, anyone pregnant or nursing, and anyone preparing for surgery should talk to their doctor before starting it.
Key takeaways
Cold weather does thicken blood, measurably: six hours in moving air at 75 °F raised whole-blood viscosity 21 percent in healthy volunteers whose core temperature fell only 0.4 °C (Keatinge 1984).
The mechanism is concentration, not more cells: two hours at 64 °F removed 14 percent of plasma volume — about two cups — mostly into the tissues, with fibrinogen and cholesterol rising in step (Neild 1994).
Cooler blood is itself thicker: in a viscometer, taking blood from 36.5 °C to 22 °C raised viscosity 26 percent, which is why cold fingers feel the effect first (Çinar 2001).
Fibrinogen runs higher in winter — 23 percent higher in the coldest six months in one cohort of over-75s — and winter colds, not only the thermometer, help explain it (Stout 1991; Woodhouse 1994).
Cold blunts thirst by up to 40 percent while driving a plasma-heavy diuresis, so winter hydration has to be planned rather than felt (Kenefick 2004; Sawka 2015).
Layer the torso, block the wind, and drink before you feel like it — that is what the cold research supports, and it costs nothing. If you also want daily support for healthy blood flow, healthy blood viscosity and circulation through the longer run of the season, Great Billiom Nattokinase 10,800 FU gives you the research-matched dose with K2 MK-7 and serrapeptase in one two-capsule serving, for $19.99.
Frequently asked questions
Does cold weather really thicken your blood?
Yes, in healthy adults and without extreme cold. Six hours in moving air at 24 °C (75 °F) raised whole-blood viscosity by 21 percent in a 1984 BMJ experiment, with packed cell volume up 7 percent and core temperature down only 0.4 °C. The change came from plasma water leaving the circulation, not from extra blood cells.
Why is blood thicker in winter?
Two reasons stack. Cold shifts water out of the plasma into the tissues and the urine, concentrating everything left behind, including fibrinogen. And winter colds raise fibrinogen through the body's inflammatory response: one year-long study of 65- to 74-year-olds found the winter rise tracked cough and inflammatory markers rather than the outdoor temperature.
How long does it take for cold to affect your blood?
Longer than an hour, shorter than an afternoon. In the six-hour 24 °C experiment, "little of these increases occurred in the first hour," with most of the change after it. Two hours in moving air at 18 °C (64 °F) was enough to remove 14 percent of plasma volume in both young and older volunteers.
Should you drink more water in cold weather?
Drink on a schedule, because thirst is not a reliable guide in the cold. Cold exposure cut thirst by up to 40 percent at rest and during moderate exercise in one trial, even when the blood's osmolality said water was needed, and cold also drives a diuresis that removes proportionally more plasma than sweating does.
Does nattokinase help with thick blood in cold weather?
No nattokinase trial has measured blood viscosity or fibrinogen after cold exposure, so this article makes no such claim. Great Billiom Nattokinase 10,800 FU is daily support for healthy blood viscosity, healthy fibrin metabolism and circulation, taken as the label directs — two capsules a day on an empty stomach. For this afternoon, the evidence points to warmth and water.
Megan Elliott, Content Editor at Great Billiom. Every claim in this article is sourced from the primary research linked above. Read our editorial standards → thegreatbilliom.com/editorial-standards
Sources
Keatinge WR, Coleshaw SR, Cotter F, Mattock M, Murphy M, Chelliah R. "Increases in platelet and red cell counts, blood viscosity, and arterial pressure during mild surface cooling: factors in mortality from coronary and cerebral thrombosis in winter." BMJ, 1984;289(6456):1405–1408.
Neild PJ, Syndercombe-Court D, Keatinge WR, Donaldson GC, Mattock M, Caunce M. "Cold-induced increases in erythrocyte count, plasma cholesterol and plasma fibrinogen of elderly people without a comparable rise in protein C or factor X." Clinical Science, 1994;86(1):43–48.
Stout RW, Crawford V. "Seasonal variations in fibrinogen concentrations among elderly people." The Lancet, 1991;338(8758):9–13.
Woodhouse PR, Khaw KT, Plummer M, Foley A, Meade TW. "Seasonal variations of plasma fibrinogen and factor VII activity in the elderly: winter infections and death from cardiovascular disease." The Lancet, 1994;343(8895):435–439.
Çinar Y, Şenyol AM, Duman K. "Blood viscosity and blood pressure: role of temperature and hyperglycemia." American Journal of Hypertension, 2001;14(5):433–438.
Kenefick RW, Hazzard MP, Mahood NV, Castellani JW. "Thirst sensations and AVP responses at rest and during exercise-cold exposure." Medicine & Science in Sports & Exercise, 2004;36(9):1528–1534.
Sawka MN, Cheuvront SN, Kenefick RW. "Hypohydration and Human Performance: Impact of Environment and Physiological Mechanisms." Sports Medicine, 2015;45(Suppl 1):S51–S60.
Chen H, et al. "Effective management of atherosclerosis progress and hyperlipidemia with nattokinase: A clinical study with 1,062 participants." Frontiers in Cardiovascular Medicine, 2022;9:964977.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Individual results may vary.
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