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No new studies since the Lon White one - and that's the reason that it should be discounted or deprecated in some way? Absence of evidence is not evidence of absence. I mean, if the study is well designed (as it apparently was), and the findings robust (as they apparently were - see dose-response), and the objections, such as they were are adequately disposed of (aluminum and production contaminants, prevalence of Alzheimer's vs vascular dementia in Japan), then sheer passage of time should not somehow undermine those attributes - those have not changed. Would it be useful if more studies came out to confirm these findings? Absolutely - but then this study can join a long line of other worthy studies that would benefit from more confirmation. That still does not invalidate those findings, unless, you know, they were invalidated - the only reason to invalidate or throw doubt upon would be if since then other studies came out that contradicted or otherwise undermined the Lon White study. I am not aware of any such. Therefore the mere passage of time is not enough in my mind to be a factor to doubt the findings of that study. Unless there is evidence to contradict the Lon White study, it strikes me as reasonable grounds to be cautious when it comes to consuming soy products.


Supplementing with vit. K2. I supplemented with K2 (MK-4 and MK-7) for 6 years. I based that not only on bone health concerns, but on purported CV effects as outlined in the Rotterdam study. But then I experienced a health issue that I laid down at least partially at the feet of K2 supplementation - admittedly I did this completely speculatively, based on nothing more than guesswork and my own reading of PubMed papers (again: completely speculative). I decided to quit supplementing with K2.


In keeping with the precautionary principle, I could not confirm the long term safety of supplementing with K2. I'm old enough to be familiar with this pattern: a given vitamin is touted as enhancing health and therefore would be great to supplement with - and then, years later, we find that in both supra-RDA and even RDA amounts, the health effects are deleterious. That list is long, and anyone is welcome to chase down studies and references: vitamin E, vitamin A, C, beta-carotene, folate, B12 and so on. Meanwhile, broad spectrum supplementation with multivitamins has not show health benefits even when taken by large numbers of people on poor diets (who could presumably benefit the most), even followed up for decades. And now a new group of optimists comes along and promises that this time, with another fat-soluble vitamin, it really is going to be different, cross my heart double promise for realz this time peeps: K2. Riiiight. Pull the other, it's got bells on it. I'm not disputing that there aren't plenty of intriguing hints about a variety of marvels that K2 can accomplish - I'm just reminding myself that the exact same thing happened before with all those other vitamins, and every single time it ended the same way. Oh, but this time it'll be different - time for a musical interlude and the immortal words of Morrissey: please enjoy "He was a sweet and tender hooligan, hooligan And he swore that he'll never, never do it again And of course he won't (oh, not until the next time)".


I am not opposed to getting some K2 in my diet - rather than through supplements. But I'd rather not do it through a soy product like Natto, or saturated-fat-laden cheese. If anyone has any practical suggestions I'm all ears.

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You are right to follow the precautionary principle. But then again, if we all do what we've always done, we'll all end up just as dead as everyone else who has ever lived. You have to cast your lot with some intervention(s), or you too will end up dying.


Regarding the soy in natto. Didn't you just speak to the weakness of the tofu dementia link by calling into question the Lon White study of elderly Hawaiian men, on the basis that it hasn't been replicated despite it coming out many years ago?


Given how rich natto is in K2, it doesn't take much to get a respectable dose of the vitamin - just a few grams. Do you really think that a few grams of fermented soybeans really has the potential to negatively impact brain health, even if the concern about tofu and dementia has any merit (which I to doubt)?



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Re: Lon White study - no, it was you, Dean who made that claim (that you've developed more doubt about the study due to the fact that it has not been replicated since). I addressed your argument in my post, and found it wanting.


You are right about needing to act on speculation and the precautionary principle cannot be absolute. I embark on speculative ventures all the time. And my speculation may be wrong. For example, my embarking on CR was a speculative endeavor, and now it transpires that CR may not work as we speculated in humans. So I'm not completely risk averse. But the soy-dementia connection is a bridge too far for me - it is not a risk I'm willing to take, based on the evidence to date, and based on my own speculation (which may transpire to be wrong, along with the Lon White study). I find the relative absence of long term studies of K2 and the kind of scrutiny other failed "star" vitamins received (f.ex. vit. E) troubling. That too strikes me as a speculative bridge too far. I'm ok with taking risks, but stop at Russian Roulette when the odds become too uncomfortable.


That is why I am not opposed - indeed welcome - more K2 in my diet, but would rather not gamble with supplemental forms (which have failed with so many vitamins before). And turning my gaze at diet, I am very uneasy about soy products and cheeses as the source of K2. You are right, the natto amounts are much smaller than customary tofu consumption, but strike me as still too much to take a risk - after all, there are more than a few bioactive substances in gram amounts that can affect our physiology. How many grams of tea do brew? That's apparently enough to cause an effect. And if small amounts of natto are enough to deliver one compound that can affect physiology (K2), then so can another (deleterious one). We don't know what exactly it is that's harmful in soy. And therefore we cannot judge what amounts may be safe.

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I hear you Tom, and I understand and respect your perspective. We're all N-of-1 experiments, and we have to pick and choose where we make our stand(s).


There definitely are other active ingredients in natto besides vitamin K2. In particular nattokinase, which appear beneficial as I discussed earlier in this thread. But it does have pretty powerful effects, and the long-term effects haven't been carefully studied.


I will note in natto's favor that, while shrouded in a bit of mystery, it has clearly been eaten in Japan since the 1600s, in much larger amounts I might add than the 1/4-carton per day that I've chosen to eat.


Ironically, that is about how long it's been since folks in the west have been eating tomatoes - before that they were believed to be poisonous. Now few of us healthy eaters go a meal without tomatoes in one form or another. Go figure. We've all got to go with the evidence available, and pick our poisons accordingly...



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Natto Once Again Shown to Increase Bone Mineral Density


Thanks to Al Pater for finding this new study [1], which found once again that vitamin K(2) and natto are associated with better bone health, this time among 500 postmenopausal Japanese women.  


From the free full text, over the 5 years between baseline and the end of the study, virtually all the women lost some bone mass - almost without exception their BMD dropped. But those women who ate the most natto (high quartile, ≥ one carton per day, N=118) lost only ½ as much bone mass as women who ate natto rarely or not at all (N=58), even after controlling for a range of potential confounding factors. In fact, there was a strong dose-response relationship between quintile of natto intake and BMD (i.e. more natto → higher BMD). A similar positive relationship was seen between BMD and dietary vitamin K (sum of K1 & K2) intake as assessed by dietary questionnaire and 3-day food log. 


Coffee, tea and alcohol intake were also positively associated with BMD, although not to the extent of either natto or vitamin K. Meat consumption was inversely associated with BMD (i.e. more meat → lower BMD).


Once again it appears the slimy soybeans have benefits for bones!





[1] Tohoku J Exp Med. 2016;239(2):95-101. doi: 10.1620/tjem.239.95.


Association between Dietary Intake and Bone Mineral Density in Japanese
Postmenopausal Women: The Yokogoshi Cohort Study.

Hirata H, Kitamura K, Saito T, Kobayashi R, Iwasaki M, Yoshihara A, Watanabe

Y, Oshiki R, Nishiwaki T, Nakamura K.

Free Full text: 


Diet and food intake play an important role in the development of
osteoporosis. However, apart from calcium and vitamin D, how nutrients
affect bone status is not fully understood. The purpose of this study was to
determine cross-sectional and longitudinal associations between dietary
intake and bone mineral density (BMD) in Japanese postmenopausal women. This
5-year cohort study included 600 community-dwelling women aged 55-74 years
at baseline in 2005. Information on demographics, nutrition, and lifestyle
was obtained through interviews, and nutritional and dietary intake was
assessed using a validated food frequency questionnaire. BMD measurements
were performed by dual energy X-ray absorptiometry. In 2010, 498 women
underwent follow-up BMD examinations. Multiple linear regression analysis
was performed to determine associations of predictor variables with BMD,
adjusting for confounders. In cross-sectional analyses, coffee or black tea
consumption was positively associated with lumbar spine (P = 0.004) and
total hip (P = 0.003) BMD, and alcohol intake was positively associated with
femoral neck (P = 0.005) and total hip (P = 0.001) BMD. In longitudinal
analyses, vitamin K (P = 0.028) and natto (fermented soybeans) (P = 0.023)
were positively associated with lumbar spine BMD, and meat or meat product
consumption was inversely associated with total hip (P = 0.047) BMD. In
conclusion, dietary factors other than calcium and vitamin D intake are
predictors of bone mass and bone loss in Japanese postmenopausal women. In
particular, natto intake is recommended for preventing postmenopausal bone
loss on the basis of current evidence.


PMID: 27238552 

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  • 6 months later...

I am not opposed to getting some K2 in my diet - rather than through supplements. But I'd rather not do it through a soy product like Natto, or saturated-fat-laden cheese. If anyone has any practical suggestions I'm all ears.


To date and after some hours of internet research, unfortunately I haven't been able to find nothing else. Actually, there might be a lot of K2 in some low-fat cheese, since the bacteria producing it feed on lactose and are indifferent to fat. Parmesan might contain lots of K2 but we don't know, there are very little analytical data in literature. Probably we might be able to get K2 in home made kefir from nonfat milk. I don't know about the taste though, I suspect it might be terrible. An option might be to drain the lowfat or nonfat kefir to obtain an homemade analog of twarog, that would likely contain significant K2 (if the starter contains lactococcus and leucostoc) and no saturated fats with acceptable palatability. I'll have to search about convenient drainings methods and maybe start producing Twarog myself.

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I've started making my own Twarog, simply by putting the home made kefir into a kitchen strain and let the water percolate. It tastes very good and can be done with lowfat milk/kefir, with a good taste as well and with an eye to saturated fats. 


In lieu of Natto, this should ensure some non-negligible amount of dietary K2 in the form mainly of MK9.



Edited by mccoy
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  • 2 years later...

Here is a new paper [1] posted by Al Pater (thanks Al!) which found eating a pack of natto per day was associated with almost a 50% reduction in osteoporotic fractures among postmenopausal Japanese women. The risk reduction was independent of bone mineral density (BMD). Notably, other soybean products weren't associated with a reduction in fracture risk. 

I take a vitamin K2 supplement, but I really need to get back to the Asian market to pick up some more natto.



[1] Natto Intake is Inversely Associated with Osteoporotic Fracture Risk in Postmenopausal Japanese Women.
Kojima A, Ikehara S, Kamiya K, Kajita E, Sato Y, Kouda K, Tamaki J, Kagamimori S, Iki M.
J Nutr. 2019 Dec 11. pii: nxz292. doi: 10.1093/jn/nxz292. [Epub ahead of print]
PMID: 31825069
The direct association between intake of Japanese fermented soybeans, namely natto, and bone mineral density (BMD) is known. However, the association with osteoporotic fractures has not been studied.
This study aimed to investigate whether habitual natto intake is associated with a risk of osteoporotic fractures.
This prospective cohort study included 1417 postmenopausal Japanese women who were enrolled in the Japanese Population-Based Osteoporosis cohort study in 1996, 1999, 2002, and 2006 and were aged ≥45 y at baseline. The intake of natto, tofu, and other soybean products was surveyed with use of a FFQ at baseline. Fractures were ascertained in follow-up surveys conducted in 1999, 2002, 2006, and 2011/2012. Osteoporotic fracture was the primary outcome and was defined as a clinical fracture occurring without strong external force, diagnosed with radiographs by a medical doctor. HRs with 95% CIs were estimated with Cox proportional hazard models.
During the 17,699 person-years of follow-up (median, 15.2 y), 172 women experienced osteoporotic fractures. After adjustment for age and BMD at the total hip, the HRs compared with those of < 1 pack (approximately 40 g)/wk natto intake were 0.72 (95% CI: 0.52, 0.98) and 0.51 (95% CI: 0.30, 0.87) for 1-6 and ≥7 packs/wk, respectively. After further adjustment for BMI, history of osteoporotic fractures, history of myocardial infarction or stroke, diabetes mellitus, current smoking, alcohol intake, frequency of tofu and other soybean product intakes, and dietary calcium intake, the HRs were 0.79 (95% CI: 0.56, 1.10) and 0.56 (95% CI: 0.32, 0.99) for 1-6 and ≥7 packs/wk, respectively. Frequency of tofu or other soybean product intakes had no association with the risk of osteoporotic fractures.
Habitual natto intake may be associated with a reduced risk of osteoporotic fractures independent of confounding factors, including BMD, in Japanese postmenopausal women. This trial was registered at umin.ac.jp as UMIN 000032869.
fermented soybeans; natto; osteoporotic fracture; postmenopausal women; prospective cohort study

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Yes, Dean, I noticed that study this morning (thanks Al!) - and wondered if anyone would comment, given the natto threads around here. But there is another study that Al posted yesterday which I've been puzzling over ever since - and in a roundabout way, it's tangentially related to the natto study. In one sense, the natto study is a morbidity and biomarker study - it tells us that you'll have less bone breakage and osteoporosis. If you go up in this thread there is also a study which recommends natto:


"In particular, natto intake is recommended for preventing postmenopausal bone
loss on the basis of current evidence."

Which says directly that natto should prevent or ameliorate osteoporosis. This is where Al's puzzling study comes in from yesterday:

Increased lifespan, decreased mortality, and delayed cognitive decline in osteoarthritis.
Mayburd AL, Baranova A.
Sci Rep. 2019 Dec 9;9(1):18639. doi: 10.1038/s41598-019-54867-8.
PMID: 31819096
In absence of therapies targeting symptomatic dementia, better understanding of the biology underlying a cognitive decline is warranted. Here we present the results of a meta-analysis of the impact of osteoarthritis (OA) on cognitive decline and overall mortality. Across 7 independent datasets obtained in studies of populations in the USA, EU and Australia (NBER, NSHAP, TILDA, NACC, Kaiser Permanente, GRIM BOOKS, OAI, with a total of >7 × 107 profiles), OA cohorts demonstrated higher cognitive scores, later dementia onset as well as longer lifespan and lower age-specific all-cause mortality. Moreover, generalized OA with multiple localizations is associated with more significant reduction of mortality and dementia than a singly localized OA or no arthritis. In OA patients with younger ages, all-cause mortality was disproportionally reduced as compared to that in controls, while exponential term of Gompert'z hazard function was increased, accelerating mortality accrual at later ages. Up to 8-10% of poly-osteoarthritic patients are predicted and observed to reach centenarian lifespan, while in matched non-OA population the same benchmark is reached by less than 1% of patients. These results point at a possibility of life-extending and cognition preserving impacts of OA-conditioned immune system.

Ain't that something? Quite a humdinger. Note, that they speculate - again speculate - as to why OA seems to be associated with life extending effects and cognition preservation (i.e. it's immune system driven). But the study can show us no grounds for such speculation - no proof of mechanism. All it can ascertain is the correlation. Why that is, who knows. 

But that effect is very robust - it is pretty astounding: 8-10% of poly-osteoarthritic patients are observed to reach centenarian lifespan, while matched non-OA population is only at 1% - that's 1000% - or TEN TIMES the rate. That's eye-wateringly high. If we were to go only with this, you should be down on your knees praying for poly-osteoarthrisis. 

Note again - we have no idea what the mechanism is in the case of OA being life prolonging/cognition preserving. And on the other side - we actually don't know what life-expansion effect natto intake has, all we have is a morbidity marker. And ironically a morbidity marker (OA and bone breakage) that's in direct opposition to lifespan, at least according to the study Al posted - which means that if you were to look at just that, you should avoid natto precisely because it inhibits OA. All you can say is that natto prevents OA - and nobody can prove that that's desirable rather than undesirable from a life-extension and cognitive preservation point of view.

Now what?

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This is very interesting, Tom. Great point.

Natto seems to also reduce the incidence of CVD, so its osteoarthritis impact may be offset by it. https://www.ncbi.nlm.nih.gov/pubmed/27927636

Or, OA may simply correlate with something else which provides a protective effect, such as lower calcium intake?

Edited by Ron Put
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Right. It's a correlation or association - anything could be responsible; perhaps calcium as you suggest; or - to be cheeky, lower intake of K2 (with the additional complication that perhaps some K2 which appears in abundance f.ex. with cheese might also mean you take in a lot of saturated fat and that's a negative etc. - so if your K2 is high, it's good for bones, but it's at the cost of taking in a lot of saturated fat which might be a negative, etc.). There are tons of confounders, so it's very difficult to know why OA is associated with lifespan/cognition preservation in such a counter-intuitive way.  But given how astoundingly huge this effect is - 10 times(!) the number of centenarians, I think it would be very useful to investigate this OA effect.

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The study you reference (PMID 31819096) linking osteoarthritis (OA) with better cognition and longevity is a real head scratcher. But I'm not following your logic relating OA and natto.

In particular, OA is not the same as osteoporosis. In fact, there is evidence that OA sufferers have a lower risk of bone fractures than non-OA sufferers [1].

So when you say:

2 hours ago, TomBAvoider said:

All you can say is that natto prevents OA - and nobody can prove that that's desirable rather than undesirable from a life-extension and cognitive preservation point of view

I don't think that follows from any evidence I've seen. Natto seems to reduce fracture risk, but this reduction is independent of bone mineral density, which is the benchmark used to diagnose osteoporosis. 

In other words, natto doesn't even seem to increase BMD and therefore reduce osteoporosis. So that's strike one against your argument. Strike two is the fact that osteoporosis /= to OA. So unless you know of evidence I haven't seen, natto doesn't seem to bear on osteoarthritis at all. In fact [2] looked at various dietary factors and their association with OA in Japanese oldsters. It found no association between natto consumption at OA. Strike three is the fact that both natto and OA appear to so something similar (i.e. reducing fracture risk) - so why avoid natto if you think OA is somehow good for you?

Furthermore, even if natto did help prevent OA (which it doesn't), I still wouldn't be inclined to hold that against natto, despite the apparent positive association between OA and cognitive health / longevity. Why? Because it seems pretty implausible to me that OA per se is protective against cognitive decline or aging. It seems much more likely that either Al's study is a fluke, or, if the associations hold up, that OA is a marker for other factors that are good for cognition / longevity.  

Here are two, non-mutually exclusive possibilities for such a marker:

1) OA appears to be associated with a more "vigilant" immune system. Perhaps OA is a marker for an immune system better able to clear out pro-aging, dementia-inducing scenescent cells, as the authors of Al's study speculate.

2) OA is associated with being overweight/obese in part through the extra stress on joints caused by carrying extra weight. Paradoxically, being overweight/obese later in life is associated with increased longevity, as we've discussed before. Perhaps OA is a marker for having more beneficial "meat on your bones" when you're older.

If you disagree, and think OA per se may be beneficial based on Al's study and are willing to put up with seriously lower quality of life that OA sufferers report, there are a few interventions you can do to help yourself develop it, including:

  • live a sedentary lifestyle
  • avoid coffee [2]!
  • become overweight/obese
  • get a knee or other joint injury
  • stop taking your statin and increase your cholesterol

Personally I'm going to give those interventions a pass.

But I agree with you that it will be interesting to look further into the apparent association between OA and better cognitive health and longevity, particularly to see if the hypothesis about better scenescent cell clearance holds up.



[1] Calcif Tissue Int. 2009 Apr;84(4):249-56. doi: 10.1007/s00223-009-9224-z. Epub

2009 Feb 23.

Osteoarthritis and risk of fractures.

Vestergaard P(1), Rejnmark L, Mosekilde L.

Author information: 
(1)Department of Endocrinology and Metabolism C, Aarhus Amtssygehus, Aarhus
University Hospital, Aarhus, Denmark. p-vest@post4.tele.dk

We conducted a case-control study on the effects of osteoarthritis (OA) on the
risk of fractures. There were 124,655 fracture cases and 373,962 age- and
gender-matched controls. The main exposure was OA, and the main confounders were 
use of diuretics, antihypertensive drugs, and pain medication. OA was associated 
with a decreased risk of any fracture and of hip, forearm, and spine fractures.
In general a decreasing trend in the risk of fractures was present with
increasing time sine diagnosis of OA. The effect on fractures in areas rich in
cortical bone such as the hip in general was larger than effects on skeletal
sites rich in trabecular bone such as the spine. OA in the hip and knee, in
general, was associated with a decreasing risk of fractures with time since
diagnosis of OA, while this was not the case for OA in other locations. OA seems 
to be associated with a decreased risk of fractures at multiple skeletal sites as
well as sites far from the location of OA
. This may indicate systemic effects on 
bone strength, especially in areas rich in cortical bone.

DOI: 10.1007/s00223-009-9224-z 
PMID: 19234808


[2] Association between Dietary Habits and Knee Osteoarthritis in Japanese Older Adults: A Cross-Sectional Study

Article · January 2013 with 9 Reads · Download citation
DOI: 10.4172/2161-0533.1000120

Kyoko Kondo
Background: To elucidate whether dietary habits affect knee osteoarthritis, we analyzed data from past regional screening programs for arthritis and osteoporosis. Methods: Subjects comprised 493 Japanese individuals (120 men, 373 women; age range, 40-83 years) who participated in a regional screening program for arthritis and osteoporosis in a single town in southwestern Japan. Outcome measure was radiographically determined knee osteoarthritis, categorized according to the criteria of Kellgren and Lawrence as grade ≥ 2, 1 or 0. Associations between dietary habits and knee osteoarthritis were assessed by calculating odds ratios and 95% confidence intervals using a proportional odds model in logistic regression. Results: Odds ratio for knee osteoarthritis was decreased with daily coffee consumption at 40 years of age (odds ratio=0.48, 95% confidence interval=0.28-0.83). Female sex (odds ratio=2.19, 95% confidence interval=1.15-4.15), age (3rd vs. 1st tertile: odds ratio=14.9, 95% confidence interval=8.07-27.5), weight at 40 years of age (3rd vs. 1st tertile: odds ratio=2.50, 95% confidence interval=1.41-4.43), previous knee injury (odds ratio=2.01, 95% confidence interval=1.24-3.24), and physical worker (odds ratio=2.09, 95% confidence interval=1.41-3.11) were significantly associated with knee osteoarthritis. Conclusions: Daily coffee consumption at 40 years of age was inversely associated with severe radiographic

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Well, there is a link between arthritis and osteoporosis - prominently the inflammatory variant:


And the study I cited does claim greater BMD for natto (see the title!) - and if you scroll up to the post you made and from which I extracted the study I referenced, you yourself titled is as such:

Natto Once Again Shown to Increase Bone Mineral Density

Now, of course I don't think that OA somehow inherently is a health-positive thing - it's an illness and quite debilitating. All I'm saying is that something odd is going on and something worth investigating.

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1 hour ago, TomBAvoider said:

Well, there is a link between arthritis and osteoporosis - prominently the inflammatory variant:


Tom, did notice the "inflammatory variants" of arthritis your link discusses does not include osteoarthritis? Hence it is irrelevant. OA, if anything, is associated with increased BMD, as I pointed out above. For a primer on the relationship between inflammatory (rheumatoid) arthritis, osteoarthritis and osteoporosis, see here. The most relevant section says:

Although osteoporosis and osteoarthritis are two very different medical conditions with little in common, the similarity of their names causes great confusion. These conditions develop differently, have different symptoms, are diagnosed differently, and are treated differently.

So even if natto does increase BMD (which it may), this doesn't in any way suggest natto will undermine whatever it is about OA that seems to be associated with cognitive health / longevity, since if anything OA is associated with increased BMD too.


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  • 5 months later...

Some sensationalist headlines, but nevertheless, a further indication of the benefits of fermented soy products, including natto, miso, and fermented soy paste:

"The researchers found that a higher intake of fermented soy was linked to a significantly lower risk of all cause mortality at 10 per cent.

Total soy intake, including products like tofu, soy milk, okara, did not effect mortality.

People who ate natto also had a lower risk of death from cardiovascular disease, such as heart disease, than those who did not eat natto.

No links were found between soy intake and cancer related deaths.  

Results persisted even after further adjusting for intake of vegetables, which was higher among those consuming larger portions of natto."

I've been wondering if the high salt content of stuff like miso doesn't diminish the effects, even if on balance the stuff is beneficial.


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  • 1 year later...

Here is a new, relatively-large, well-designed, three-year randomized control trial of nattokinase supplements for cardiovascular health in healthy older people at low risk of CVD [1]. It basically found nattokinase to be ineffective.

Here are the main tables from the paper, showing nattokinase (2000 FU/day) had no significant impact on a wide range of measures of cardiovascular health, including arterial thickness or stiffness, cholesterol, glucose, insulin, blood pressure, or various measurements of blood coagulation tendency:





So if you are taking a nattokinase supplement for its potential to improve cardiovascular health, it looks like it probably isn't worth it. One concern we previously discussed was the potential for nattokinase to act as a blood thinner which might be bad for CR folks with already thin blood, which could trigger bleeding/stroke. That doesn't look like a problem.

The author's acknowledged that the cohort was healthier and the dose was lower than previous studies which hinted at potential benefits of nattokinase for cardiovascular health. But the demographics and dosage of this study seems quite relevant for folks here. The authors also said natto contains other active compounds besides nattokinase, but the thought has been that it would be the nattokinase (if anything) in natto that would positively influence CVD due to its pharmokinetics and animal experiments.

The study doesn't address the two other potential benefits of eat natto, i.e. brain health (for its potential to break up amyloid plaques) and bone health (from its high level of vitamin K2).



[1]  Clinical Hemorheology and Microcirculation, vol. Pre-press, no. Pre-press, pp. 1-15, 2021

Nattokinase Atherothrombotic Prevention Study: A randomized controlled trial

Authors: Hodis, Howard N.a; b; c; * | Mack, Wendy J.a; c | Meiselman, Herbert J.d | Kalra, Vijaye | Liebman, Howardb | Hwang-Levine, Julianaa; b | Dustin, Lauriec | Kono, Naokoc | Mert, Melissac | Wenby, Rosalinda B.d | Huesca, Emilianoe | Rochanda, Leanneb | Li, Yanjiea | Yan, Mingzhua | St. John, Jan Aa; c | Whitfield, Loraa

Abstract: BACKGROUND:Described to be antithrombotic and antihypertensive, nattokinase is consumed for putative cardiovascular benefit. However, no large-scale, long-term cardiovascular study has been conducted with nattokinase supplementation. OBJECTIVE:To determine the effect of nattokinase on subclinical atherosclerosis progression and atherothrombotic biomarkers. METHODS:In this double-blinded trial, 265 individuals of median age 65.3 years, without clinical evidence of cardiovascular disease (CVD) were randomized to oral nattokinase 2,000 fibrinolytic units or matching placebo. Primary outcome was rate of change in subclinical atherosclerosis measured by serial carotid ultrasound every 6 months as carotid artery intima-media thickness (CIMT) and carotid arterial stiffness (CAS). Additional outcomes determined at least every 6 months were clinical parameters including blood pressure and laboratory measures including metabolic factors, blood rheology parameters, blood coagulation and fibrinolysis factors, inflammatory markers and monocyte/macrophage cellular activation markers. RESULTS:After median 3 years of randomized treatment, annualized rate of change in CIMT and CAS did not significantly differ between nattokinase supplementation and placebo. Additionally, there was no significant effect of nattokinase supplementation on blood pressure or any laboratory determination. CONCLUSIONS:Results of this trial show that nattokinase supplementation has a null effect on subclinical atherosclerosis progression in healthy individuals at low risk for CVD.

DOI: 10.3233/CH-211147

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16 hours ago, Ron Put said:

Interesting, thanks.

I still eat natto (store-bought) about 4 times per week, I have grown to kind of like it. Never really disliked it in the first place, but many seem to.

As to supplements, well, another one bites the dust.

It’s seems the vast majority bite the dust sooner or later.

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