Jump to content

Recommended Posts

Does anyone else eat natto, the fermented soybean product which is quite popular in Japan?

 

It is the richest food source of vitamin K2 (menaquinone-7 or MK-7) with 1 mg (1000 mcg) of K2 per 100g natto. That is about 20x higher than the next highest source, certain cheeses like Gouda. Unlike vitamin K1 which is found primarily in leafy greens, there is virtually no vitamin K2 in regular fruits and vegetables.

 

Why should we care about vitamin K2 you ask?

 

First and foremost because it has been shown to be protective against osteoporosis [1-2], a concern for CR practitioners. From [2], a study of 244 postmenopausal women supplemented with 180mcg/day of Vitamin K2 (MK-7) for three years: 

 

MK-7 intake significantly improved vitamin K status and decreased the
age-related decline in BMC and BMD at the lumbar spine and femoral neck, but not
at the total hip. Bone strength was also favorably affected by MK-7. MK-7
significantly decreased the loss in vertebral height of the lower thoracic region
at the mid-site of the vertebrae.
 
CONCLUSIONS: MK-7 supplements may help postmenopausal women to prevent bone loss.

 

Another significant benefit of Vitamin K2 is for cardiovascular health. Vitamin K2 seems to prevent artery calcification (aka hardening of the arteries) [3-5], which happens when calcium circulating in the blood is turned into a crust in the arteries. In study [5] the same group of researchers from [2] measured arterial calcification in the same 244 postmenopausal women on 180mcg/day of K2 for three years, and found multiple markers of arterial stiffness improved with K2 supplementation, concluding:

 

Long-term use of MK-7 supplements improves arterial stiffness in healthy
postmenopausal women, especially in women having a high arterial stiffness.

 

But those were studies of direct supplementation of vitamin K2 (MK-7), rather than getting it from food. Does eating natto actually raise serum MK-7 levels? Thankfully the answer is yes, according to [6]:

 

erum MK-7 level with the frequency of dietary natto intake were examined in 134
healthy adults (85 men and 39 women) without and with occasional (a few times per
month), and frequent (a few times per week) dietary intake of regular natto
including MK-7 (775 micrograms/100 g). Serum MK-7 and gamma-carboxylated
osteocalcin concentrations in men with the occasional or frequent dietary intake
of natto were significantly higher than those without any intake. 

 

So where to get natto?

 

I buy my natto in frozen form at my local asian market, for about $2.50 for four styrofoam containers each of which contains about 50g of natto. Here is what the package of four look like:

 

1326223910natto.jpg

 

I eat half of a container's worth of natto per day (cost ~ $0.30/day). That 25g of natto per day provides about 250mcg of Vitamin K2 (MK-7), which is about 30% more than the dose shown to improve bone health [2] and reduce arterial stiffness [5] in postmenopausal women.

 

What's natto like you ask?

 

There is no getting around the fact that it looks pretty gross, and has a very slimy texture. As a result, many people can't stomach it, but I actually enjoy the taste, especially when mixed into the serving of other legumes and starches I eat. Below is a photo of natto in the styrofoam container. Pretty appetizing, huh?! The chopsticks in the photo are helpful for scale:

 

natto_scoop.jpg

 

For those of you who would be too grossed out by natto to eat it, there are supplements available. In fact I take one of these* to increase my K2 beyond what I get from natto - adding an extra 100mcg MK-7 per day for $0.09. But I'm always in favor of getting nutrients from food sources when practical. This is one of the rare cases where the natural food source is price competitive with supplement sources. So for me natto is a good choice.

 

Does anyone else eat natto? If not, you might consider giving it a try!

 

[Note: This post does not address Natto's brain health benefits. For discussion of that, see this post further down this thread.]

 

--Dean

 

*Note - I've updated my supplement regime to this vegan NOW Foods brand K2 supplement, to make sure I'm getting K2 in MK-7 form, rather than (mostly) MK-4 per my previous supplement.

 

---------

[1] J Bone Miner Metab. 2014 Mar;32(2):142-50. doi: 10.1007/s00774-013-0472-7. Epub

2013 May 24.

Low-dose vitamin K2 (MK-4) supplementation for 12 months improves bone metabolism
and prevents forearm bone loss in postmenopausal Japanese women.

Koitaya N(1), Sekiguchi M, Tousen Y, Nishide Y, Morita A, Yamauchi J, Gando Y,
Miyachi M, Aoki M, Komatsu M, Watanabe F, Morishita K, Ishimi Y.

Author information:
(1)Department of Food Function and Labeling, National Institute of Health and
Nutrition, 1-23-1 Toyama, Shinjyuku-ku, Tokyo, Japan.

Menaquinone-4 (MK-4) administered at a pharmacological dosage of 45 mg/day has
been used for the treatment of osteoporosis in Japan. However, it is not known
whether a lower dose of MK-4 supplementation is beneficial for bone health in
healthy postmenopausal women. The aim of this study was to examine the long-term
effects of 1.5-mg daily supplementation of MK-4 on the various markers of bone
turnover and bone mineral density (BMD). The study was performed as a randomized,
double-blind, placebo-controlled trial. The participants (aged 50-65 years) were
randomly assigned to one of two groups according to the MK-4 dose received: the
placebo-control group (n = 24) and the 1.5-mg MK-4 group (n = 24). The baseline
concentrations of undercarboxylated osteocalcin (ucOC) were high in both groups
(>5.1 ng/ml). After 6 and 12 months, the serum ucOC concentrations were
significantly lower in the MK-4 group than in the control group. In the control
group, there was no significant change in serum pentosidine concentrations.
However, in the MK-4 group, the concentration of pentosidine at 6 and 12 months
was significantly lower than that at baseline. The forearm BMD was significantly
lower after 12 months than at 6 months in the control group. However, there was
no significant decrease in BMD in the MK-4 group during the study period. These
results suggest that low-dose MK-4 supplementation for 6-12 months improved bone
quality in the postmenopausal Japanese women by decreasing the serum ucOC and
pentosidine concentrations, without any substantial adverse effects.

PMID: 23702931

 

------------

[2] Osteoporos Int. 2013 Sep;24(9):2499-507. doi: 10.1007/s00198-013-2325-6. Epub

2013 Mar 23.

Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in
healthy postmenopausal women.

Knapen MH(1), Drummen NE, Smit E, Vermeer C, Theuwissen E.

Author information:
(1)VitaK, Maastricht University, Oxfordlaan 70, 6229 EV, Maastricht, The
Netherlands.

We have investigated whether low-dose vitamin K2 supplements (menaquinone-7,
MK-7) could beneficially affect bone health. Next to an improved vitamin K
status, MK-7 supplementation significantly decreased the age-related decline in
bone mineral density and bone strength. Low-dose MK-7 supplements may therefore
help postmenopausal women prevent bone loss.INTRODUCTION: Despite contradictory
data on vitamin K supplementation and bone health, the European Food Safety
Authorities (EFSA) accepted the health claim on vitamin K's role in maintenance
of normal bone. In line with EFSA's opinion, we showed that 3-year high-dose
vitamin K1 (phylloquinone) and K2 (short-chain menaquinone-4) supplementation
improved bone health after menopause. Because of the longer half-life and greater
potency of the long-chain MK-7, we have extended these investigations by
measuring the effect of low-dose MK-7 supplementation on bone health.
METHODS: Healthy postmenopausal women (n = 244) received for 3 years placebo or
MK-7 (180 μg MK-7/day) capsules. Bone mineral density of lumbar spine, total hip,
and femoral neck was measured by DXA; bone strength indices of the femoral neck
were calculated. Vertebral fracture assessment was performed by DXA and used as
measure for vertebral fractures. Circulating uncarboxylated osteocalcin (ucOC)
and carboxylated OC (cOC) were measured; the ucOC/cOC ratio served as marker of
vitamin K status. Measurements occurred at baseline and after 1, 2, and 3 years
of treatment.
RESULTS: MK-7 intake significantly improved vitamin K status and decreased the
age-related decline in BMC and BMD at the lumbar spine and femoral neck, but not
at the total hip. Bone strength was also favorably affected by MK-7. MK-7
significantly decreased the loss in vertebral height of the lower thoracic region
at the mid-site of the vertebrae.
CONCLUSIONS: MK-7 supplements may help postmenopausal women to prevent bone loss.
Whether these results can be extrapolated to other populations, e.g., children
and men, needs further investigation.

PMID: 23525894

 

-----------

[3] Acta Physiol Hung. 2010 Sep;97(3):256-66. doi: 10.1556/APhysiol.97.2010.3.2.

Vitamin K and vascular calcifications.

Fodor D(1), Albu A, Poantă L, Porojan M.

Author information:
(1)University of Medicine and Pharmacy, 2nd Internal Medicine, Clinic Iuliu
Hatieganu, Cluj-Napoca, Romania. dfodor@umfcluj.ro

The role of vitamin K in the synthesis of some coagulation factors is well known.
The implication of vitamin K in vascular health was demonstrated in many surveys
and studies conducted over the past years on the vitamin K-dependent proteins
non-involved in coagulation processes. The vitamin K-dependent matrix Gla protein
is a potent inhibitor of the arterial calcification, and may become a
non-invasive biochemical marker for vascular calcification. Vitamin K(2) is
considered to be more important for vascular system, if compared to vitamin K(1).
This paper is reviewing the data from recent literature on the involvement of
vitamin K and vitamin K-dependent proteins in cardiovascular health.

PMID: 20843764

 

----------------

[4] Nutrients. 2015 Aug 18;7(8):6991-7011. doi: 10.3390/nu7085318.

High-Dose Menaquinone-7 Supplementation Reduces Cardiovascular Calcification in a
Murine Model of Extraosseous Calcification.

Scheiber D(1), Veulemans V(2), Horn P(3), Chatrou ML(4), Potthoff SA(5), Kelm
M(6,)(7), Schurgers LJ(8), Westenfeld R(9).

Author information:
(1)Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty,
University Duesseldorf, Duesseldorf 40225, Germany.
daniel.scheiber@med.uni-duesseldorf.de. (2)Division of Cardiology, Pulmonology,
and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf
40225, Germany. verena.veulemanns@med.uni-duesseldorf.de. (3)Division of
Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University
Duesseldorf, Duesseldorf 40225, Germany. patrick.horn@med.uni-duesseldorf.de.
(4)Department of Biochemistry, Cardiovascular Research Institute Maastricht,
Maastricht University, Maastricht 6229 ER, The Netherlands.
m.chatrou@maastrichtuniversity.nl. (5)Department of Nephrology, University
Duesseldorf, Medical Faculty, Duesseldorf 40225, Germany.
sebastian.potthoff@med.uni-duesseldorf.de. (6)Division of Cardiology,
Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf,
Duesseldorf 40225, Germany. malte.kelm@med.uni-duesseldorf.de. (7)Cardiovascular
Research Institute Duesseldorf, University Duesseldorf, Medical Faculty,
Duesseldorf 40225, Germany. malte.kelm@med.uni-duesseldorf.de. (8)Department of
Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht
University, Maastricht 6229 ER, The Netherlands.
l.schurgers@maastrichtuniversity.nl. (9)Division of Cardiology, Pulmonology, and
Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf 40225,
Germany. ralf.westenfeld@med.uni-duesseldorf.de.

Cardiovascular calcification is prevalent in the aging population and in patients
with chronic kidney disease (CKD) and diabetes mellitus, giving rise to
substantial morbidity and mortality. Vitamin K-dependent matrix Gla-protein (MGP)
is an important inhibitor of calcification. The aim of this study was to evaluate
the impact of high-dose menaquinone-7 (MK-7) supplementation (100 µg/g diet) on
the development of extraosseous calcification in a murine model. Calcification
was induced by 5/6 nephrectomy combined with high phosphate diet in rats. Sham
operated animals served as controls. Animals received high or low MK-7 diets for
12 weeks.
We assessed vital parameters, serum chemistry, creatinine clearance,
and cardiac function. CKD provoked increased aortic (1.3 fold; p < 0.05) and
myocardial (2.4 fold; p < 0.05) calcification in line with increased alkaline
phosphatase levels (2.2 fold; p < 0.01). MK-7 supplementation inhibited
cardiovascular calcification and decreased aortic alkaline phosphatase tissue
concentrations. Furthermore, MK-7 supplementation increased aortic MGP messenger
ribonucleic acid (mRNA) expression (10-fold; p < 0.05). CKD-induced arterial
hypertension with secondary myocardial hypertrophy and increased elastic fiber
breaking points in the arterial tunica media did not change with MK-7
supplementation. Our results show that high-dose MK-7 supplementation inhibits
the development of cardiovascular calcification
. The protective effect of MK-7
may be related to the inhibition of secondary mineralization of damaged vascular
structures.

PMCID: PMC4555157
PMID: 26295257

 

-------------

[5] Thromb Haemost. 2015 May;113(5):1135-44. doi: 10.1160/TH14-08-0675. Epub 2015 Feb

19.

Menaquinone-7 supplementation improves arterial stiffness in healthy
postmenopausal women. A double-blind randomised clinical trial.

Knapen MH, Braam LA, Drummen NE, Bekers O, Hoeks AP, Vermeer C(1).

Author information:
(1)Cees Vermeer, PhD, VitaK, Maastricht University, Biopartner Center Maastricht,
Oxfordlaan 70, 6229 EV Maastricht, The Netherlands, Tel: +31 43 388 5865, Fax:
+31 43 388 5889, E-mail: c.vermeer@vitak.com.

Observational data suggest a link between menaquinone (MK, vitamin K2) intake and
cardiovascular (CV) health. However, MK intervention trials with vascular
endpoints are lacking. We investigated long-term effects of MK-7 (180 µg
MenaQ7/day) supplementation on arterial stiffness in a double-blind,
placebo-controlled trial. Healthy postmenopausal women (n=244) received either
placebo (n=124) or MK-7 (n=120) for three years. Indices of local carotid
stiffness (intima-media thickness IMT, Diameter end-diastole and Distension) were
measured by echotracking. Regional aortic stiffness (carotid-femoral and
carotid-radial Pulse Wave Velocity, cfPWV and crPWV, respectively) was measured
using mechanotransducers. Circulating desphospho-uncarboxylated matrix
Gla-protein (dp-ucMGP) as well as acute phase markers Interleukin-6 (IL-6),
high-sensitive C-reactive protein (hsCRP), tumour necrosis factor-α (TNF-α) and
markers for endothelial dysfunction Vascular Cell Adhesion Molecule (VCAM),
E-selectin, and Advanced Glycation Endproducts (AGEs) were measured. At baseline
dp-ucMGP was associated with IMT, Diameter, cfPWV and with the mean z-scores of
acute phase markers (APMscore) and of markers for endothelial dysfunction
(EDFscore). After three year MK-7 supplementation cfPWV and the Stiffness Index
βsignificantly decreased in the total group, whereas distension, compliance,
distensibility, Young's Modulus, and the local carotid PWV (cPWV) improved in
women having a baseline Stiffness Index β above the median of 10.8. MK-7
decreased dp-ucMGP by 50 % compared to placebo, but did not influence the markers
for acute phase and endothelial dysfunction. In conclusion, long-term use of MK-7
supplements improves arterial stiffness in healthy postmenopausal women,
especially in women having a high arterial stiffness.


PMID: 25694037

 

----------

[6] J Bone Miner Metab. 2000;18(4):216-22.

Intake of fermented soybean (natto) increases circulating vitamin K2
(menaquinone-7) and gamma-carboxylated osteocalcin concentration in normal
individuals.

Tsukamoto Y(1), Ichise H, Kakuda H, Yamaguchi M.

Author information:
(1)Central Research Institute, Mitsukan Group Co., Ltd., Aichi, Japan.

Changes in circulating vitamin K2 (menaquinone-7, MK-7) and gamma-carboxylated
osteocalcin concentrations in normal individuals with the intake of fermented
soybeans (natto) were investigated. Eight male volunteers were given sequentially
fermented soybeans (natto) containing three different contents of MK-7 at an
interval of 7 days as follows: regular natto including 775 micrograms/100 g (MK-7
x 1) or reinforced natto containing 1298 micrograms/100 g (MK-7 x 1.5) or 1765
micrograms/100 g (MK-7 x 2). Subsequently, it was found that serum MK-7 and
gamma-carboxylated osteocalcin concentrations were significantly elevated
following the start of dietary intake of MK-7 (1298 or 1765 micrograms/100 g).
Serum undercarboxylated osteocalcin concentrations were significantly decreased
by dietary MK-7 (1765 micrograms/100 g) supplementation. Moreover, the changes in
serum MK-7 level with the frequency of dietary natto intake were examined in 134
healthy adults (85 men and 39 women) without and with occasional (a few times per
month), and frequent (a few times per week) dietary intake of regular natto
including MK-7 (775 micrograms/100 g). Serum MK-7 and gamma-carboxylated
osteocalcin concentrations in men with the occasional or frequent dietary intake
of natto were significantly higher than those without any intake. The present
study suggests that intake of fermented soybean (natto) increases serum levels of
MK-7 and gamma-carboxylated osteocalcin in normal individuals.

PMID: 10874601

Edited by Dean Pomerleau
Changed thread title to include brain health and link to brain health post

Share this post


Link to post
Share on other sites

Hi Dean:

 
Natto?  Gosh, I thought you'd never ask!

 

When I am in close enough proximity to a good oriental grocery store (not currently) I eat a package a week of natto.

 

You have to get used to the taste (dijon mustard disguises it well) as well as its appearance.

  

I read somewhere that the japanese think it such an important food they now require it to be available in school lunches.

   

Rodney. 

 

==========

 

"The unverified conventional wisdom is almost invariably mistaken."

Edited by nicholson

Share this post


Link to post
Share on other sites

You have to get used to the taste [of natto] (dijon mustard disguises it well) as well as its appearance.

  

I read somewhere that the japanese think it such an important food they now require it to be available in school lunches.

 

Yes - spicing it up makes a big different in palatability!

 

Regarding the attitude of Japanese people to natto, from the natto wikipedia page:

 

A 2009 internet survey in Japan indicated 70.2% of respondents like nattō and 29.8% do not, but out of 29.8% who dislike nattō, about half of them eat nattō for its health benefits.

 

Probably a self-selected and therefore biased sample, but still a pretty impressive fraction of natto eaters!

 

--Dean

Share this post


Link to post
Share on other sites

I don't eat natto, but Mike Linksvayer does, as (I believe) does Tadd Ottman.

 

Q: Dean, some years back you took an hiatus from natto proper due to concerns about soy-induced brain rot; instead, you had ingeniously begun making your own natto using peas instead of soybeans as the feedstock. Have you abandoned that, and if so, why? Or did it just fall by the wayside during the period when health concerns were not a major driver for your CR practice?

Share this post


Link to post
Share on other sites

Michael,

 

Back then I had no source of real natto, so I tried making my own using peas instead of soybeans. But I was never quite sure how well my pea-based natto was fermenting. And it was a pain in the butt! So I stopped trying to make my own pea-natto years ago.

 

Recently I discovered inexpensive, frozen natto in the Asian grocery store where I shop to get my durian fix. :-)

 

Regarding soy and brain rot. I'm still pretty skeptical of the evidence against tofu, and the more time that passes without corroborating evidence, the more skeptical I get. But I'm avoiding tofu per your cautions just to be safe.

 

But my daily natto intake is less than an ounce, probably about a half oz of that being actual soybeans. I seriously doubt that such a small a dose of soy (without the aluminum or formaldehyde potentially associated with tofu) is going to negatively impact my brain, even if there is a issue with tofu.

 

Dean

Share this post


Link to post
Share on other sites

I might add that, since many nutrients - particularly vitamins - are in effect catalysts (I don't know if K2 is) you do not need a huge amount of them for your intake to be adequate. 

 

So a carton of natto a week may be plenty to fulfil its purpose.  Possibly just one carton a month?  But I don't know, and would be interested in input about, optimal quantity.

 

Rodney.

 

============

 

"The unverified conventional wisdom is almost invariably mistaken."

Edited by nicholson

Share this post


Link to post
Share on other sites

So a carton of natto a week may be plenty to fulfil its purpose.  Possibly just one carton a month?  But I don't know, and would be interested in input about, optimal quantity.

 

Rodney,

 

I've been investigating natto further today, and in particular its other active component, nattokinase (NK). I won't detail all the research on NK here. It is spelled out pretty well on these two web sites, each of which has lots of references to back up the findings I'll summarize here.

  • A standard dose of purified NK used in most studies is about the amount in one 50g carton of natto.
  • A significant portion of NK ingested as natto or in purified capsule for can get through the stomach and be absorbed into the bloodstream. 
  • Once in the bloodstream, it can act as a pretty potent blood thinner & clot buster. 
  • It also reduces blood pressure by about 5.5 mmHg / 3 mmHg if taken in about that dose for a month.
  • It also breaks up amyloids, implicated in a bunch of degenerative diseases, including Alzheimer's disease [1] (see reference below for quotes), although whether NK can get through the blood-brain barrier in unclear.

So rather than rotting your brain (as has been tentatively suggested for tofu), natto (via NK) may actually help break up the accumulation of crud in the brain associated with Alzheimer's disease. But that is speculation. I will note though, that the natto- and tofu-loving Japanese have a rate of Alzheimer's disease that is 11x lower than the US. Suggestive I would say...

 

Regardless, natto is clearly a very functional food. Perhaps a bit too functional, particularly when it comes to blood thinning.

 

As you suggest, I'm thinking of cutting back on my 25g/day, to a lower dose of around 12.5g/day, just to be safe.

 

[Note: Here is the text of a much longer post I started composing for anyone interested, with references, but gave up in favor of this summary and pointers to the web pages with references instead.]

 

--Dean

 

-----------

[1] J Agric Food Chem. 2009 Jan 28;57(2):503-8. doi: 10.1021/jf803072r.

Amyloid-degrading ability of nattokinase from Bacillus subtilis natto.

 

Hsu RL(1), Lee KT, Wang JH, Lee LY, Chen RP.

 
PMID: 19117402
 

More than 20 unrelated proteins can form amyloid fibrils in vivo which are

related to various diseases, such as Alzheimer's disease, prion disease, and

systematic amyloidosis. Amyloid fibrils are an ordered protein aggregate with a

lamellar cross-beta structure. Enhancing amyloid clearance is one of the targets

of the therapy of these amyloid-related diseases. Although there is debate on

whether the toxicity is due to amyloids or their precursors, research on the

degradation of amyloids may help prevent or alleviate these diseases. In this

study, we explored the amyloid-degrading ability of nattokinase, a fibrinolytic

subtilisin-like serine protease, and determined the optimal conditions for

amyloid hydrolysis. This ability is shared by proteinase K and subtilisin

Carlsberg, but not by trypsin or plasmin.

 

Quotes from full text:

 

In this study, we used three kinds of in vitro prepared amyloid fibrils, A40 amyloid fibrils, insulin amyloid fibrils, and huPrP (consisting prion sequence 108-144) amyloid fibrils, to test the amyloid-degrading ability of nattokinase.

 

After treatment of the three different amyloid fibrils with nattokinase, the amyloid signal was decreased (Figures 1 and 2), indicating the general amyloid-degrading ability of nattokinase.

 

This amyloid-degrading ability of nattokinase suggests that it may be useful in the treatment of amyloid-related diseases.

 

The discovery of an enzyme which can be safely taken orally and can degrade amyloid fibrils could be very useful in the therapy of amyloid related diseases. Nattokinase not only dissolved blood clots (9) but also degraded amyloid fibrils. Our amyloid-degrading studies demonstrated that it is active at neutral pH and body temperature. Previous results in rats, dogs, and humans have suggested that nattokinase can enter the circulation when taken orally (11, 12), so it has the potential to clear amyloid deposits in various parts of the body.

 

Moreover, since natto has been ingested by humans for a long time, it would be worthwhile to carry out an epidemiological study on the rate of occurrence of various amyloid-related diseases in a population regularly consuming natto.

 

Share this post


Link to post
Share on other sites

I've been investigating natto further today, and in particular its other active component, nattokinase (NK). ...

  • A significant portion of NK ingested as natto or in purified capsule for can get through the stomach and be absorbed into the bloodstream.
  • Once in the bloodstream, it can act as a pretty potent blood thinner & clot buster.

These have are actually lead me long to suggest that people on CR avoid natto(kinase), because we already have very low haemostatic tone due to CR itself and (usually) actually having adequate (or even generous or excessive) omega-3 intake. This overall lowers our risk of CVD events, but the more you thin out the blood the greater the risk of haemorrhagic stroke or a bad outcome in case of an accident.

 

  • It also reduces blood pressure by about 5.5 mmHg / 3 mmHg if taken in about that dose for a month.

I would be surprised if it had this effect in people on CR with our (usually) extremely low BP — or that if it did, a pharmacological-type BP lowering would necessarily be beneficial.

 

  • It also breaks up amyloids, implicated in a bunch of degenerative diseases, including Alzheimer's disease [1].

Ye-e-eah. First, the amyloids they looked at were beta-amyloid(1-40) (which is widely considered to be the much less harmful and possibly harmless or in some cases beneficial Abeta species: it's the much more aggregate-prone Abeta(1-42) that appears to do the harm)); prion protein amyloid (an issue in mad cow disease and Creutzfeld-Jacob, but likely not worth worrying about for the vast majority of humanity); and insulin fibrils (which is a problem in the pharmaceutical biosynthesis and purification of insulin, and in very rare cases at the site of frequent insulin injections in diabetics, but not for the rest of us).

 

Second, they performed the degradation in phosphate buffer solution: this is not a crazy thing to do as a preliminary test, but at minimum you want to see if it can still interact in the presence of human serum. No such data.

 

Third, NK is a 27.7 kDa protein. The standard test for a badly-breached blood-brain barrier is 10 kDa-size dextran. I shudder to think of the poor soul with a BBB that screwed up, unless there is some specific transporter that NK would use to enter the brain — and then, I'd want to know what else it might degrade.

 

Now, there is a perfectly plausible mechanism whereby cleavage of systemic Abeta could ultimately lower brain Abeta, by "osmotically" drawing more soluble Abeta out of the brain (the so-called "peripheral sink" phenomenon). But (a) to be effective, it would have to target Abeta(1-42), which is a tougher nut tot crack and which they've not shown it can cleave, and (b) it would have to do this under physiological conditions, which (again) they've not taken the first step toward demonstrating.

 

So rather than rotting your brain (as has been tentatively suggested for tofu), natto (via NK) may actually help break up the accumulation of crud in the brain associated with Alzheimer's disease. But that is speculation.

You may recall that historically, until the recent "Westernization" of the diet, Alzheimer's was a far less common form of dementia in Japan: the more common form was a form of vascular dementia, inverting the pattern in the West. And the cognitive decline linnked to tofu in the White et al study was associated with brain atrophy, with no data one way or t'other on amyloid accumulation.

 

 

-----------

[1] http://pubs.acs.org/doi/abs/10.1021/jf803072r

Share this post


Link to post
Share on other sites

Thanks Michael,

 

I agree with you that the blood thinning and blood pressure lowering effects of nattokinase (NK) are unlikely to be beneficial for most CR practitioners, although there are notable exceptions who've recently posted about their BP being uncomfortably elevated... In fact, as you suggest, the blood thinning effects could indeed be deleterious - resulting in excessive bleeding as a result of an accident or stroke. So certainly NK (and natto) is something to be cautious about, at the very least.

 

Now, regarding what I'm most interested in, namely the potential dementia-prevention benefits of NK, via its demonstrated ability to break up at least some types of beta-amyloid plaques, some types of which being implicated in Alzheimer's disease. Given your role in the SENS research project, where breaking up accumulated 'gunk' like beta-amyloid inside and outside of cells is key to your strategy for defeating aging, I take your insights in this area wrt NK very seriously. If you say it is unlikely that NK would be beneficial for brain health by clearing beta-amyloid gunk based on the evidence you've seen, then I trust your judgment.

 

But...

 

Investigating NK's impact on the brain, I came across this recent (2013) study [1]. These researchers induced a model of Alzheimer's disease (AD) in adult rats by feeding them aluminum chloride for 45 days (aluminum is suspected, although not unequivocally demonstrate, to be involved in the etiology of AD in people). The rats treated with aluminum suffered from increased markers of brain inflammation, reduced BDNF and IGF-1 (which are good for maintaining/repairing neurons), as well as outright neurodegeneration and amyloid-beta plaque formation in the hippocampus. In short, aluminum messes up the rats' brains in a way that very much resembles AD in humans. As far as I understand it, this aluminum-fed rat paradigm is a pretty widely used model of human Alzheimer's disease.

 

In parallel with the 45 days of aluminum feeding, the researchers fed the mice one of two compounds they thought might counteract the aluminum-induced AD-like pathology. One of these compounds was NK, literally fed to them in the form of this Doctor's Best NK supplement, available from Amazon. I'll ignore the other (serrapeptase), although it is also a supplement available from Doctor's Best...

 

The amount of NK fed to the rats was either low-dose (360 FU/kg bw / day) or high dose (720 FU / kg bw / day). How much natto does this translate too? Quite a bit, but not a huge amount, if I understand things correctly. Using this procedure to convert from rat to human dose, the low dose NK of 360 FU / kg bw / day in rats, equates to about 4000 FU per day in a 150lb human. So the low dose was the human equivalent of two of the Doctor's Best NK capsules per day, or two 50g styrofoam cartons of natto per day. The high NK dose was twice that, or four cartons of natto per day. Recall I'm eating between 1/4 and 1/2 carton per day. So these rats are getting quite a bit, but not an unreasonably large amount of NK per day - about the equivalent of 8-16x as much as is in the natto I'm currently eating per day.

 

So what did the find in the brains of rats with the equivalent of AD who were fed the NK?

 

From the abstract:

Oral administration of ... NK in a rat model of AD daily for 45 days resulted in a significant decrease in brain AchE activity, TGF-β, Fas and IL-6 levels [markers of inflammation and other bad stuff going on in the brain]. Also, the treatment with these enzymes produced significant increase in BDNF and IGF-1 levels [compounds that help with healthy brain maintenance & repair] when compared with the untreated AD-induced rats. Moreover, ... NK could markedly increase the expression levels of ADAM9 and ADAM10 genes in the brain tissue of the treated rats [two genes that produce proteins that are known to help break up amyloid-beta plaques]. These findings were well confirmed by the histological examination of the brain tissue of the treated rats. The present results support our hypothesis that the oral administration of proteolytitc enzyme... NK, would have an effective role in modulating certain factors characterizing AD. Thus, [this enzyme] may have a therapeutic application in the treatment of AD.

 

Looking at the full text, the mention of "well confirmed by the histological examination of the brain tissue of the treated rats" translates to the following:

 

Treatment of AD group with a low dose of NK
(360 Fu/ kg bw) for 45 days revealed an obvious
improvement in the histology of different brain areas
associated with the lysis of amyloid plaques in the
hippocampus. Treatment of
AD group with a high dose of NK (720 Fu/kg bw)
resulted in the disappearance of amyloid plaques in
the hippocampus.
 
Basically, the formation of the amyloid plaques in the hippocampus was either greatly attenuated and/or they were broken up effectively by the NK.
 
In short, by all their metrics, it appears that 45 days of a physiologically-relevant oral dose of NK markedly improved the brain health of the rats induced with AD-like pathology.
 
Here is the proposed mechanism for all these benefits as described by the researchers:
 
NK possesses high amyloid degrading
ability, which suggests the usefulness of
this enzyme in the treatment of amyloid-related
diseases.3 Thus, these enzymes might dissolve Ab [amyloid-beta]
protein that accumulates in the brain due to aluminium
neurotoxicity. This explanation was well documented
by our histological findings (Figures 6©). As mentioned
above, Ab plays an important role in the activation
of AchE activity in the brain
besides its reducing effect on brain BDNF content.
Therefore, the degradation of Ab by these enzymes
leads to the inhibition of brain AchE activity and
restoration of BDNF brain level. Moreover, the dissolution
of Ab by ... [the] NK enzyme results in the
blocking of the inflammatory cascade and preventing
the production of the proinflammatory cytokines such
as TGF-b and IL-6 in the brain. Also, the elimination
of Ab deposits helps in correcting the disruption of
brain IGF-1 level and managing the process of apoptosis
and neuronal death due to the suppressing of Fas
expression and in turn its level in the brain.
 
These results indicate that th[is] enzyme may
have the ability to shift the amyloidogenic pathway
to the non-amyloidogenic one via increasing the
expression level of ADAM9 and ADAM10 genes in
the brain. To the best of the author’s knowledge, this
is the first published study that highlighted the efficacy
of ... NK in alleviating the generation
of Ab in the brain via promoting the activity of
a-secretase-like action.
 
 

Obviously it is just one study in rats. But the results appear pretty promising.

 

Michael, what do you think?

 

--Dean

 

----------

[1] Hum Exp Toxicol. 2013 Jul;32(7):721-35. doi: 10.1177/0960327112467040.

Serrapeptase and nattokinase intervention for relieving Alzheimer's disease
pathophysiology in rat model.

Fadl NN(1), Ahmed HH, Booles HF, Sayed AH.
 

Free (although pirated via Sci-Hub.io) Full Text: http://het.sagepub.com.sci-hub.io/content/32/7/721.short

 

Serrapeptase (SP) and nattokinase (NK) are proteolytic enzymes belonging to
serine proteases. In this study, we hypothesized that SP and NK could modulate
certain factors that are associated with Alzheimer's disease (AD) pathophysiology
in the experimental model. Oral administration of aluminium chloride (AlCl3) in a
dose of 17 mg/kg body weight (bw) daily for 45 days induced AD-like pathology in
male rats with a significant increase in brain acetylcholinesterase (AchE)
activity, transforming growth factor β (TGF-β), Fas and interleukin-6 (IL-6)
levels. Meanwhile, AlCl3 supplementation produced significant decrease in
brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1)
when compared with control values. Also, AlCl3 administration caused significant
decline in the expression levels of disintegrin and metalloproteinase domain 9
(ADAM9) and a disintegrin and metalloproteinase domain 10 (ADAM10) genes in the
brain. Histological investigation of brain tissue of rat model of AD showed
neuronal degeneration in the hippocampus and focal hyalinosis with cellular as
well as a cellular amyloid plaques formation. Oral administration of SP or NK in
a rat model of AD daily for 45 days resulted in a significant decrease in brain
AchE activity, TGF-β, Fas and IL-6 levels. Also, the treatment with these enzymes
produced significant increase in BDNF and IGF-1 levels when compared with the
untreated AD-induced rats. Moreover, both SP and NK could markedly increase the
expression levels of ADAM9 and ADAM10 genes in the brain tissue of the treated
rats. These findings were well confirmed by the histological examination of the
brain tissue of the treated rats. The present results support our hypothesis that
the oral administration of proteolytitc enzymes, SP and/or NK, would have an
effective role in modulating certain factors characterizing AD. Thus, these
enzymes may have a therapeutic application in the treatment of AD.

PMID: 23821590

Share this post


Link to post
Share on other sites

To taunt Michael into possibly responding  :)xyz, two new studies point to the importance of beta-amyloid plaques in causing Alzheimer's disease (AD), rather than just being a side-effect of neurons dying for some other reason, as some previous researchers have suggested.

 

In the first study [1], discussed in this popular account, and this one, and in a cool video, found in a mouse model of AD, beta-amyloid in the brain basically formed a cast or exoskeleton around the blood vessels supplying oxygen and other nutrients to neurons, restricting their ability to respond to changes in oxygen requirements, and therefore, the authors speculate, may contribute to the oxygen deprivation that is known to cause the death of neurons in AD patients. At the end of the video, the author speculates about the possibility that new drugs for breaking up amyloids under development might prevent this destructive process. If the study of the nattokinase enzyme from natto discussed above is right, it also might be able to break up amyloid plaque in the brain, preventing this process as well.

 

The second study [2], discussed in this popular account, found that the beta-amyloid protein in AD causes synapses in hippocampal neurons to be destroyed, likely causing some of the memory and cognitive deficients so characteristic of AD. Again, perhaps natto(kinase) could help by breaking up the amyloid proteins.

 

This idea of breaking up amyloids in the brain and elsewhere as a way to combat one form of aging is important enough that the SENS Research Foundation has an entire research program underway called AmyloSENS to study how it might be accomplished...  ;)xyz

 

--Dean

 

 

--------

[1] Brain. 2015 Dec;138(Pt 12):3716-33. doi: 10.1093/brain/awv327. Epub 2015 Nov 23.

Vascular amyloidosis impairs the gliovascular unit in a mouse model of
Alzheimer's disease.

Kimbrough IF(1), Robel S(1), Roberson ED(2), Sontheimer H(3).

Cool video Abstract: http://brain.oxfordjournals.org/content/138/12/3716

Reduced cerebral blood flow impairs cognitive function and ultimately causes
irreparable damage to brain tissue. The gliovascular unit, composed of neural and
vascular cells, assures sufficient blood supply to active brain regions.
Astrocytes, vascular smooth muscle cells, and pericytes are important players
within the gliovascular unit modulating vessel diameters. While the importance of
the gliovascular unit and the signals involved in regulating local blood flow to
match neuronal activity is now well recognized, surprisingly little is known
about this interface in disease. Alzheimer's disease is associated with reduced
cerebral blood flow. Here, we studied how the gliovascular unit is affected in a
mouse model of Alzheimer's disease, using a combination of ex vivo and in vivo
imaging approaches. We specifically labelled vascular amyloid in living mice
using the dye methoxy-XO4. We elicited vessel responses ex vivo using either
pharmacological stimuli or cell-specific calcium uncaging in vascular smooth
muscle cells or astrocytes. Multi-photon in vivo imaging through a cranial window
allowed us to complement our ex vivo data in the presence of blood flow after
label-free optical activation of vascular smooth muscle cells in the intact
brain. We found that vascular amyloid deposits separated astrocyte end-feet from
the endothelial vessel wall. High-resolution 3D images demonstrated that vascular
amyloid developed in ring-like structures around the vessel circumference,
essentially forming a rigid cast. Where vascular amyloid was present, stimulation
of astrocytes or vascular smooth muscle cells via ex vivo Ca(2+) uncaging or in
vivo optical activation produced only poor vascular responses. Strikingly, vessel
segments that were unaffected by vascular amyloid responded to the same extent as
vessels from age-matched control animals. We conclude that while astrocytes can
still release vasoactive substances, vascular amyloid deposits render blood
vessels rigid and reduce the dynamic range of affected vessel segments. These
results demonstrate a mechanism that could account in part for the reduction in
cerebral blood flow in patients with Alzheimer's
disease.media-1vid110.1093/brain/awv327_video_abstractawv327_video_abstract.

PMID: 26598495

 

---------

[2]  Nature Communications, (2015) 8836. DOI: 10.1038/ncomms9836  

 

Aβ-dependent reduction of NCAM2-mediated synaptic adhesion contributes to synapse loss in Alzheimer’s disease.

 

Leshchyns’ka, I., Liew, H., Shepherd, C., Halliday, G., Stevens, C., Ke, Y., Ittner, L., & Sytnyk, V. 

 

Abstract

 

Alzheimer’s disease (AD) is characterized by synapse loss due to mechanisms that remain poorly understood. We show that the neural cell adhesion molecule 2 (NCAM2) is enriched in synapses in the human hippocampus. This enrichment is abolished in the hippocampus of AD patients and in brains of mice overexpressing the human amyloid-β (Aβ) precursor protein carrying the pathogenic Swedish mutation. Aβ binds to NCAM2 at the cell surface of cultured hippocampal neurons and induces removal of NCAM2 from synapses. In AD hippocampus, cleavage of the membrane proximal external region of NCAM2 is increased and soluble extracellular fragments of NCAM2 (NCAM2-ED) accumulate. Knockdown of NCAM2 expression or incubation with NCAM2-ED induces disassembly of GluR1-containing glutamatergic synapses in cultured hippocampal neurons. Aβ-dependent disassembly of GluR1-containing synapses is inhibited in neurons overexpressing a cleavage-resistant mutant of NCAM2. Our data indicate that Aβ-dependent disruption of NCAM2 functions in AD hippocampus contributes to synapse loss.

Share this post


Link to post
Share on other sites

It seems that everyday (literally) a new study is coming out implicating amyloid-beta in Alzheimer's Disease (AD) via a variety of mechanisms. In this new study [1], published yesterday in Nature, and discussed here, researchers investigated the relationship between the BRCA1 gene, amyloid-beta, and AD. 

 

As you may know, BRCA1 stands for BReast CAncer genes 1, and it is a knockout mutation in this gene that Angelina Jolie has, causing her to be highly prone to developing breast and/or ovarian cancer, both of which she had removed in order to avoid cancer. BRCA1 acts to repair double strand DNA breakages, one of most serious forms of DNA damage. 

 

It appears that BRCA1 is important for maintaining DNA integrity in the brain too, something that was apparently not known prior to this study, where it was thought BRCA1 only repaired double-strand breakages in frequently dividing cells, which neurons are not. Further they found BRCA1 is depleted in both AD patients and mice prone to the mouse equivalent of AD. They found that when mice explore a novel environment, their neuronal activity in memory forming areas of the brain increase, and as a result more double-strand DNA breakages occur, and the BRCA1 gene is upregulated to create more mRNA and more proteins to repair the damage. 

 

But they found the presence of amyloid-beta seems to cause the depletion of BRCA1, preventing the critical repair of these double-strand DNA breakages, which in turned seemed to impair memory and learning, at least in their mice.

 

More evidence that amyloid-beta is important in the causal pathway of the neuron death and cognitive impairment associated with AD. 

 

Getting back to the topic of this thread, natto, and one of its primary physiologically active components, nattokinase, may be able to break up blood clots in the circulatory system and amyloid-beta plaques in the brain, as discussed above. I found this clinical trial being conducted currently by researchers at the U. of Southern California to test exactly that. They are comparing 2000 FU/day of nattokinase (equiv. to one carton of natto per day) vs. placebo for three years in 240 healthy older people, in term of cardiovascular health (as measured by carotid artery intima-media thickness and stiffness) and in terms of cognitive health (via a battery of cognitive tests). It will be interesting to see the results. Unfortunately the study won't be completed until 2019...

 

The other interesting amyloid-related information I came across today was a reminder than the oldest of the old (supercentenarians) most frequently die of amyloid accumulation in the heart and circulatory system. Michael wrote about the problem, and the SENS Foundation's efforts to find a way to cleanup such amyloid buildup in this SENS research blog post. Michael focuses on the downside of existing approaches to removing amyloid using the patient's own immune system to sequester & remove it, suggesting that cleaving (breaking up) the amyloids would likely be a better strategy. I wonder Michael, do you think nattokinase might cleave the TTR amyloids that are the cause of these cardiac disorders in the very old?

 

In the meantime, I'm eating a small amount (1/4 carton) of natto per day, unless/until Michael convinces me otherwise :)xyz .

 

--Dean

 

--------------

[1] Nature Communications 6, Article number: 8897 doi:10.1038/ncomms9897

Received 06 March 2015 Accepted 14 October 2015 Published 30 November 2015
 
DNA repair factor BRCA1 depletion occurs in Alzheimer brains and impairs cognitive function in mice
 
Elsa Suberbielle, Biljana Djukic, Mark Evans, Daniel H. Kim, Praveen Taneja, Xin Wang, Mariel Finucane, Joseph Knox, Kaitlyn Ho, Nino Devidze, Eliezer Masliah & Lennart Mucke
 
 
Abstract
 
Maintaining DNA integrity is vital for all cells and organisms. Defective DNA repair may contribute to neurological disorders, including Alzheimer’s disease (AD). We found reduced levels of BRCA1, but not of other DNA repair factors, in the brains of AD patients and human amyloid precursor protein (hAPP) transgenic mice. Amyloid-β oligomers reduced BRCA1 levels in primary neuronal cultures. In wild-type mice, knocking down neuronal BRCA1 in the dentate gyrus caused increased DNA double-strand breaks, neuronal shrinkage, synaptic plasticity impairments, and learning and memory deficits, but not apoptosis. Low levels of hAPP/Amyloid-β overexpression exacerbated these effects. Physiological neuronal activation increased BRCA1 levels, whereas stimulating predominantly extrasynaptic N-methyl-D-aspartate receptors promoted the proteasomal degradation of BRCA1. We conclude that BRCA1 is regulated by neuronal activity, protects the neuronal genome, and critically supports neuronal integrity and cognitive functions. Pathological accumulation of Aβ depletes neuronal BRCA1, which may contribute to cognitive deficits in AD.

Share this post


Link to post
Share on other sites

I'm pretty skeptical of Dr. Mercola's advice, seeing him as one step up from Dr Oz... But in this case, his article on K2 has some pretty good information and  references on the benefits of vitamin K2 for bone and cardiovascular health. His advice is to either eat 4oz of raw fermented cheese per day (~400kcal & 20g of saturated fat - something I don't recommend) or to take a K2 supplement. He dismissed getting his recommended vitamine K2 dose (150mcg/day) from 15g of natto, saying:

 

You could actually get loads of MK-7 [the best form of vitamin K2] from consuming natto as it is relatively inexpensive, and is available in most Asian food markets. Few people, however, tolerate its smell and slimy texture.

 

Don't be discouraged by Mercola's disparaging remarks - give natto a try. And while you're at your local asian market being adventuresome, pick up some durian too!

 

--Dean

Share this post


Link to post
Share on other sites

Thanks, Dean! I've never tried natto -- for some odd reason I was worried about sodium and processing. Now because of your natto clarion call I'll give it a chew around the block...

Share this post


Link to post
Share on other sites

Are you concerned at all about the "significant increase in IGF-1 levels" described in the study you quoted from?  I thought low IGF-1 levels were desirable as one of the key pathways associated with longevity?  Just a layman's thought I had, but perhaps the k2/natto regimen is best left until you are older when IGF-1 levels are naturally lower (for example start that when you are >75 years old? 

 

 

Share this post


Link to post
Share on other sites

Gordo,

 

Regarding the increased levels of IGF-1 with natto(kinase) treatment in rats in PMID: 23821590.

 

Notice the increased IGF-1 was in the brains of nattokinase fed rats, where, like BDNF, it is reduced in AD, and where it can be very helpful for maintenence and repair.

 

So while the evidence suggest you want relatively low levels of IGF-1 circulating in your blood for increased longevity and to avoid cancer, in the brain IGF-1 is likely a good thing. In fact, one of the main concerns with keeping IGF-1 too low is the potential long-term impact on cognition, because IGF-1 is important for brain health.

 

So if I can keep IGF-1 low in my blood, while eating small amounts of natto to preferentially keep IGF-1 levels reasonable in my brain, I'd consider that a win-win.

 

--Dean

 

Share this post


Link to post
Share on other sites

Dean - you briefly mentioned making natto (with peas?).  I've done a bit of reading on making natto, and it doesn't seem very difficult.  Quick summary -- cook soybeans or buy them precooked, mix with regular commercial natto as your starter, spread over a pan, stick in oven with a small light bulb (incubator if you have one) targetting 100-115 degrees F, leave for 24-36 hours, done.

 

I bought a bunch of different brands, so far they all taste the same to me, and all "string up" nicely when stirred vigorously, not sure what the difference is supposed to be between the $4 3-pack and the $1.50 3-pack, haha.  But the market that sells this is quite far for me, and it just seems more economical to make it myself and occasionally buy new starter from the market.  Just curious if anyone is doing that and how it has worked out?

Share this post


Link to post
Share on other sites

Gordo,

 

Years ago, before I even knew the Asian market near my house carried frozen natto, I did make it myself using peas rather than soybeans. As I recall, it never got quite as stringy as the store-bought stuff I get now. Its pretty easy to buy the natto starter spores on-line. Here is where I got mine. I'll be curious if you try it and how it works.

 

For me, I visit the asian market every 5 weeks or so, and pick up two frozen 4-packs for about $2.50 each. That's about $0.63 per styrofoam pack, and each one lasts me 4 days, so it costs me about $0.15/day to eat my tiny serving of natto. That's cheap enough that I don't mind paying it, to save the hassle of trying to incubate my own. Heck, the 15-watt light bulb I'd have to use in the incubator alone costs in the neighborhood of $0.04/day for electricity to run.

 

--Dean

Share this post


Link to post
Share on other sites

How'd you determine a 1/4 serving a day was right for you?

 

I don't think I'd buy spores, when I could just dump one cheap container of store bought natto into a pan with a bunch of soybeans, mix it all up, and maybe end up with 10x quantity of natto (?) after a day or 2.  4 cents of electricity in exchange for not having to drive 2 hours might be worth it to me, I don't know yet.  I'll probably try it at least once. 

Share this post


Link to post
Share on other sites

Gordo,

 

How'd you determine a 1/4 serving a day was right for you?

 

I explain my (not completely rigorous) rationale in this post earlier in the thread.

 

2 hours is a long drive. Fortunately my Asian market is only 20min away, and I shop there every few weeks anyway to buy durian and other staples :-).

 

--Dean

Share this post


Link to post
Share on other sites

All,

 

Here is another recent study [1] showing the benefits of natto and vitamin K2 (specifically in the Menaquinone-7 or MK-7 form). In a double blind, placebo controlled clinical trial, researchers found that MK-7 supplements (100 mcg/day) reduced rheumatoid arthritis symptoms and markers of inflammation that accompany it, including the familiar and important marker of imflammation C-Reactive Protein (CRP).

 

For anyone whose chicken to eat natto, or doesn't have an Asian grocery store nearby, you can get the same 100 mcg/day dose of the MK-7 form of vitamin K2 in one capsule of this Now supplement

 

--Dean

 

---------

[1] Eur J Pharmacol. 2015 Aug 15;761:273-8. doi: 10.1016/j.ejphar.2015.06.014. Epub

2015 Jun 11.
 
Menaquinone-7 as a novel pharmacological therapy in the treatment of rheumatoid
arthritis: A clinical study.
 
Abdel-Rahman MS(1), Alkady EA(2), Ahmed S(3).
 
Author information: 
(1)Department of Pharmacology and Toxicology, College of Pharmacy, Taibah
University, Al Madinah AlMunawarah 30001, Saudi Arabia; Department of
Pharmacology, Faculty of Medicine, Assiut University, Assiut, Egypt. Electronic
address: mahran44@hotmail.com. (2)Department of Rheumatology & Rehabilitation,
Faculty of Medicine, Assiut University, Assiut, Egypt. (3)Department of
Pharmacognosy and Pharmaceutical Chemistry, College of Pharmacy, Taibah
University, Al Madinah AlMunawarah 30001, Saudi Arabia; Department of
Pharmaceutical Analytical Chemistry, Faculty of Pharmacy, Assiut University,
Assiut 71526, Egypt.
 
Menaquinones (MKs) have been reported to induce apoptosis in rheumatoid arthritis
(RA) synovial cells. Recently, menaquinone-4 (MK-4) was proven as a new potential
agent for the treatment of RA. However, menaquinone-7 (MK-7) has greater
bioavailability and efficacy than MK-4 after oral administration. Yet, the
therapeutic benefits of MK-7 in the management of patients with RA have never
been addressed. This study was designed to clarify the therapeutic role of MK-7
added to normal therapeutic regimen of RA in patients with different stages of
the disease with a clinical follow up through a randomized clinical trial. In a
cross sectional study, 84 RA patients (24 male, 60 female) (average age=47.2
years) were enrolled in this study. The patients were divided into MK-7 treated
group (n=42) and MK-7 naïve group (n=42). MK-7 capsules were administered in a
dose of 100µg/day for three months in the first group without changing in other
medications. The clinical and biochemical markers on RA patients treated with
MK-7 and naïve group were assessed. In MK-7 treated group, serum concentrations
of MK-7 were monitored before and after three months of MK-7 administration. In
the cross sectional study, a significant decrease in MK-7 treated group for the
levels of undercarboxylated osteocalcin (ucOC), erythrocyte sedimentation rate
(ESR), disease activity score assessing 28 joints with ESR (DAS28-ESR),
C-reactive protein (CRP) and matrix metalloproteinase (MMP-3) was found. In MK-7 
treated group, a marked decrease in RA clinical and biochemical markers for
moderate and good response compared to non-responders was observed in ucOC, ESR
and DAS28-ESR. A marked increase in the levels of MK-7 for the moderate and good 
responders compared to non-responders was observed. The results suggest that MK-7
improves disease activity in RA patients. Therefore, MK-7 represents a new
promising agent for RA in combination therapy with other disease modifying
antirheumatic drugs.
 
Copyright © 2015 Elsevier B.V. All rights reserved.
 
PMID: 26073022

Share this post


Link to post
Share on other sites

Do you keep your natto frozen (like weird ice cream) before chewing on them? Reason I ask is I bought several cartons thinking I'd eat them soon, but then started fasting. They sat in the refrigerator, I opened one carton, and I don't know. These things are such an acquired taste that I'm not qualified here to judge the rancid from the okie-dokie.

Share this post


Link to post
Share on other sites

Sthira,

 

I only visit the Asian market every 5-6 weeks, so I store most of my natto cartons in the freezer. I take one out the day before I need it, and then eat 1/4 of the carton each day. I seriously doubt your carton has gone bad, unless you've stored it in your fridge for several weeks. Definitely an acquired taste though....

 

--Dean

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now

×