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Michael R

QUESTIONS & COMMENTS THREAD for " Nutrition and Supplementation for Veg(etari)ans"

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All:

First: Randy, David: thanks for the comments and questions. Do please note that I had asked:
 

Finally: this is a multi-part article, and unlike posts on the old CR Society email distribution lists, it can be periodically updated thanks to the fine editability of the Forums. To avoid cluttering up the article, please post ask any questions or comments about the contents of this article in a new thread, rather than by hitting "reply" to posts in this one. I will make a good-faith effort to answer such and to update this article as appropriate.


So I've opened up this parallel thread to answer your comments and questions. With your permission, I'd like to ask Tim to use his moderator power to delete your originals from the thread that I wanted reserved for the essay itself. Please indicate if this is agreeable.

Now:
 

"There are absolutely no natural, plant-based foods that contain vitamin B12."

I don't think that this statement is true. Please see:

www.ncbi.nlm.nih.gov/pmc/articles/PMC4042564/


First: David, please do me and you and everyone on the Forum a favor: register on the Forums and log in each time before you post! It's fine if you want to use a pseudonym, but registering and logging in will ensure that you can't be impersonated and will make it easier to keep track of your questions, input, and progress.

 

To answer your question: this Japanese group is the most proiminent in recent years to make these claims, measuring B12 levels in nori seaweed and various exotic (to Westerners) mushrooms using HPLC assays which for most things are quite reliable. However, there have been several studies (eg. (1-3)) measuring not just the levels of ostensible B12 in these foods and the blood of people eating them, but to see if doing so actually improves their functional B12 status, as measured by methylmalonic acid levels and similar assays; they have consistently been found not to do so. Thus, either (a) these compounds, too, are inactive corrinoids that happen to bear a very similar HPLC signature to true bioactive B12, or less likely ( B) there really is a small quantity of bioactive B12  in these foods, but its activity is counteracted by the much higher levels of B12-mimicking corrinoids which act as competitive inhibitors for true B12. Either way, there is no way for vegans to sustain B12-dependent metabolic pathways on purely plant-based foods, and vegans need a supplemental source of B12 to avoid dangerous deficiency.
 

Much, much thanks for you efforts in the above.
I've wanted to see a comprehensive post on this topic, and your input fits the bill.


I'm glad you found it useful. Randy, I had the definite impression that you ate meat; are you vegan, or just curious?
 

Really sad for me to see so little input from all my friends from the prior email list.
I hope, at least, they are reading.

Remember, the List had gotten pretty darned quiet, aside from postings of Al Pater's source material, for some time; I'd give them time to sort themselves out and start joining the conversation. But I strongly second your call: Old Timers from the List: come on in — the water's fine!

 

References

1: Yamada K, Yamada Y, Fukuda M, Yamada S. Bioavailability of dried asakusanori (Porphyra tenera) as a source of Cobalamin (Vitamin B12). Int J Vitam Nutr Res. 1999 Nov;69(6):412-8. PubMed PMID: 10642899.

 

2: Dagnelie PC, van Staveren WA, van den Berg H. Vitamin B-12 from algae appears not to be bioavailable. Am J Clin Nutr. 1991 Mar;53(3):695-7. Erratum in: Am J Clin Nutr 1991 Apr;53(4):988. PubMed PMID: 2000824.

 

3: Schwarz J, Dschietzig T, Schwarz J, Dura A, Nelle E, Watanabe F, Wintgens KF, Reich M, Armbruster FP. The influence of a whole food vegan diet with Nori algae and wild mushrooms on selected blood parameters. Clin Lab. 2014;60(12):2039-50. PubMed PMID: 25651739.

Edited by Michael R

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I'm glad you found it useful. Randy, I had the definite impression that you ate meat; are you vegan, or just curious?

 

reply:

Yes, I do still eat  meat and some dairy but my diet is plant heavy.

 

Regards

Randy

 

 

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So I've opened up this parallel thread to answer your comments and questions. With your permission, I'd like to ask Tim to use his moderator power to delete your originals from the thread that I wanted reserved for the essay itself. Please indicate if this is agreeable.

 

Sure, no problems. Fine with me. 

Still getting use to the new format.

 

Randy

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I hadn't had time yet to read Michael Rae's post with the attention it deserved. However, thank you tremendously for sharing all the information. That is a fantastic article, very helpful - and it answered many questions I had.

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Michael,

 

In the your terrific post about veg(etari)an nutrition and supplements, you categorize creatine as one of the few "conditionally essential" nutrients that might be beneficial for veg(etari)ans to supplement, for muscle and perhaps even brain performance. You understandably put all kinds of disclaimers around that statement, which I appreciate and acknowledge.

 

I'm wondering if you saw this new study [1] which came out after you made that post, that seems to suggest an increase in the rate of progression of Parkinson's disease in a clinical trial testing creatine if they were also consumers of caffeine.  Of course these were people who were already suffering from a serious disorder (PD), but still, I, along with virtually everyone else, use caffeine liberally, and would I would hate to undermine my brain health as a result of the combination...

 
Interesting creatine alone appears not to positively or negatively impact the rate of PD progression [2], and while [1] found no benefit (or harm) for PD from caffeine alone (or creatine for that matter), other studies have found caffeine to improve motor performance in PD patients [3]. But the two together (caffeine + creatine) seem deleterious for PD, at least according to [1].
 
Adult onset CR may protect against Parkinson's(-like) motor impairment, per this discussion, but since Roy died of some form of motor neurodegenerative disease, I've always harbored a bit of concern, and would hate to undermine any possible CR benefits for brain health through harmful supplement interactions. Of course, I don't recommend going so far as to take up smoking to ward off PD, despite the fact that there appears pretty unequivocal evidence that smoking reduced PD risk, which (ironically and purely coincidentally) was the topic of Dr. Greger's video today.
 
I'm not sure how much stock to put in any of these studies especially since [1] was in people who already had  PD, but I'm wondering if you've considered it, and whether you take creatine yourself these days.
 
James, I noticed in this post that you supplement with creatine. I'd be interested in hearing your thoughts too, especially since we are unlikely to hear from Michael if he remains true to his recent form ☹.
 
Thanks,
 
--Dean
 
--------
[1] Clin Neuropharmacol. 2015 Sep-Oct;38(5):163-9. doi: 10.1097/WNF.0000000000000102.
 
Caffeine and Progression of Parkinson Disease: A Deleterious Interaction With
Creatine.
 
Simon DK(1), Wu C, Tilley BC, Wills AM, Aminoff MJ, Bainbridge J, Hauser RA,
Schneider JS, Sharma S, Singer C, Tanner CM, Truong D, Wong PS.
 
 
OBJECTIVE: Increased caffeine intake is associated with a lower risk of Parkinson
disease (PD) and is neuroprotective in mouse models of PD. However, in a previous
study, an exploratory analysis suggested that, in patients taking creatine,
caffeine intake was associated with a faster rate of progression. In the current 
study, we investigated the association of caffeine with the rate of progression
of PD and the interaction of this association with creatine intake.
METHODS: Data were analyzed from a large phase 3 placebo-controlled clinical
study of creatine as a potentially disease-modifying agent in PD. Subjects were
recruited for this study from 45 movement disorders centers across the United
States and Canada. A total of 1741 subjects with PD participated in the primary
clinical study, and caffeine intake data were available for 1549 of these
subjects. The association of caffeine intake with rate of progression of PD as
measured by the change in the total Unified Parkinson Disease Rating Scale score 
and the interaction of this association with creatine intake were assessed.
RESULTS: Caffeine intake was not associated with the rate of progression of PD in
the main analysis, but higher caffeine intake was associated with significantly
faster progression among subjects taking creatine.
CONCLUSIONS: This is the largest and longest study conducted to date that
addresses the association of caffeine with the rate of progression of PD. These
data indicate a potentially deleterious interaction between caffeine and creatine
with respect to the rate of progression of PD.
 
PMCID: PMC4573899 [Available on 2016-09-01]
PMID: 26366971 
 
-------------
[2]  JAMA. 2015 Feb 10;313(6):584-93. doi: 10.1001/jama.2015.120.
 
Effect of creatine monohydrate on clinical progression in patients with Parkinson
disease: a randomized clinical trial.
 
Writing Group for the NINDS Exploratory Trials in Parkinson Disease (NET-PD)
Investigators, Kieburtz K(1), Tilley BC(2), Elm JJ(3), Babcock D(4), Hauser R(5),
Ross GW(6), Augustine AH(1), Augustine EU(1), Aminoff MJ(7), Bodis-Wollner IG(8),
Boyd J(9), Cambi F(10), Chou K(11), Christine CW(7), Cines M(12), Dahodwala
N(13), Derwent L(14), Dewey RB Jr(15), Hawthorne K(16), Houghton DJ(17), Kamp
C(1), Leehey M(18), Lew MF(16), Liang GS(19), Luo ST(2), Mari Z(20), Morgan
JC(21), Parashos S(22), Pérez A(2), Petrovitch H(6), Rajan S(2), Reichwein S(13),
Roth JT(7), Schneider JS(23), Shannon KM(24), Simon DK(25), Simuni T(26), Singer 
C(27), Sudarsky L(28), Tanner CM(19), Umeh CC(28), Williams K(26), Wills AM(28).
 
IMPORTANCE: There are no treatments available to slow or prevent the progression 
of Parkinson disease, despite its global prevalence and significant health care
burden. The National Institute of Neurological Disorders and Stroke Exploratory
Trials in Parkinson Disease program was established to promote discovery of
potential therapies.
OBJECTIVE: To determine whether creatine monohydrate was more effective than
placebo in slowing long-term clinical decline in participants with Parkinson
disease.
DESIGN, SETTING, AND PATIENTS: The Long-term Study 1, a multicenter,
double-blind, parallel-group, placebo-controlled, 1:1 randomized efficacy trial. 
Participants were recruited from 45 investigative sites in the United States and 
Canada and included 1741 men and women with early (within 5 years of diagnosis)
and treated (receiving dopaminergic therapy) Parkinson disease. Participants were
enrolled from March 2007 to May 2010 and followed up until September 2013.
INTERVENTIONS: Participants were randomized to placebo or creatine (10 g/d)
monohydrate for a minimum of 5 years (maximum follow-up, 8 years).
MAIN OUTCOMES AND MEASURES: The primary outcome measure was a difference in
clinical decline from baseline to 5-year follow-up, compared between the 2
treatment groups using a global statistical test. Clinical status was defined by 
5 outcome measures: Modified Rankin Scale, Symbol Digit Modalities Test, PDQ-39
Summary Index, Schwab and England Activities of Daily Living scale, and
ambulatory capacity. All outcomes were coded such that higher scores indicated
worse outcomes and were analyzed by a global statistical test. Higher summed
ranks (range, 5-4775) indicate worse outcomes.
RESULTS: The trial was terminated early for futility based on results of a
planned interim analysis of participants enrolled at least 5 years prior to the
date of the analysis (n = 955). The median follow-up time was 4 years. Of the 955
participants, the mean of the summed ranks for placebo was 2360 (95% CI,
2249-2470) and for creatine was 2414 (95% CI, 2304-2524). The global statistical 
test yielded t1865.8 = -0.75 (2-sided P = .45). There were no detectable
differences (P < .01 to partially adjust for multiple comparisons) in adverse and
serious adverse events by body system.
CONCLUSIONS AND RELEVANCE: Among patients with early and treated Parkinson
disease, treatment with creatine monohydrate for at least 5 years, compared with 
placebo did not improve clinical outcomes. These findings do not support the use 
of creatine monohydrate in patients with Parkinson disease.
TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00449865.
 
PMCID: PMC4349346
PMID: 25668262
 
 
 
---------------
[3] Neurology. 2012 Aug 14;79(7):651-8. doi: 10.1212/WNL.0b013e318263570d. Epub 2012 
Aug 1.
 
Caffeine for treatment of Parkinson disease: a randomized controlled trial.
 
Postuma RB(1), Lang AE, Munhoz RP, Charland K, Pelletier A, Moscovich M, Filla L,
Zanatta D, Rios Romenets S, Altman R, Chuang R, Shah B.
 
Author information: 
(1)Department of Neurology, McGill University, Montreal General Hospital,
Montreal, Canada. ronald.postuma@mcgill.ca
 
Erratum in
    Neurology. 2012 Oct 16;79(16):1744.
 
Comment in
    Neurology. 2012 Aug 14;79(7):616-8.
 
OBJECTIVE: Epidemiologic studies consistently link caffeine, a nonselective
adenosine antagonist, to lower risk of Parkinson disease (PD). However, the
symptomatic effects of caffeine in PD have not been adequately evaluated.
METHODS: We conducted a 6-week randomized controlled trial of caffeine in PD to
assess effects upon daytime somnolence, motor severity, and other nonmotor
features. Patients with PD with daytime somnolence (Epworth >10) were given
caffeine 100 mg twice daily ×3 weeks, then 200 mg twice daily ×3 weeks, or
matching placebo. The primary outcome was the Epworth Sleepiness Scale score.
Secondary outcomes included motor severity, sleep markers, fatigue, depression,
and quality of life. Effects of caffeine were analyzed with Bayesian hierarchical
models, adjusting for study site, baseline scores, age, and sex.
RESULTS: Of 61 patients, 31 were randomized to placebo and 30 to caffeine. On the
primary intention-to-treat analysis, caffeine resulted in a nonsignificant
reduction in Epworth Sleepiness Scale score (-1.71 points; 95% confidence
interval [CI] -3.57, 0.13). However, somnolence improved on the Clinical Global
Impression of Change (+0.64; 0.16, 1.13, intention-to-treat), with significant
reduction in Epworth Sleepiness Scale score on per-protocol analysis (-1.97;
-3.87, -0.05). Caffeine reduced the total Unified Parkinson's Disease Rating
Scale score (-4.69 points; -7.7, -1.6) and the objective motor component (-3.15
points; -5.50, -0.83). Other than modest improvement in global health measures,
there were no changes in quality of life, depression, or sleep quality. Adverse
events were comparable in caffeine and placebo groups.
CONCLUSIONS: Caffeine provided only equivocal borderline improvement in excessive
somnolence in PD, but improved objective motor measures. These potential motor
benefits suggest that a larger long-term trial of caffeine is warranted.
CLASSIFICATION OF EVIDENCE: This study provides Class I evidence that caffeine,
up to 200 mg BID for 6 weeks, had no significant benefit on excessive daytime
sleepiness in patients with PD.
 
PMCID: PMC3414662
PMID: 22855866

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Huh ... that's certainly a somewhat disturbing finding. And it's nested inside of randomized controlled trials, not just epidemiology of the creatine-using population (who are, obviously, very different in multiple respects from the general coffee-drinking population).

 

There are important distinctions here, however. In both the full-scale trial analysis (PMID 26366971) and the previous one of the Phase II trial (22855866), the dose of creatine was 10 g/day, on top of dietary intake: I think we can safely assume that there were not dramatically more veg(etari)ans in either of these trials than in the general population (ie, <3% prevalence), and likely fewer since people with PD are both of an older cohort and less in control of their diets than a random sample of the general population.

 

By contrast, we're here talking about using creatine (and the other nutrients in my article) as a supplement in the proper sense of the word, to do little more than bring veg(etari)ans' low intakes in line with the normal omnivorous dietary intake — ie, essentially, the intakes of the controls in these studies, in whom the epidemiology suggests a long-term protective effect of caffeine.

 

It may also be relevant that all of the subjects in the large trial were on dopaminergic therapy, which is the standard of care for managing the main motor symptoms but is suspected of itself hastening the disease.

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Good point Michael. Thanks.

 

It seems like modest dosing of creatine in those likely to have low levels to begin with (i.e. vegans/vegetarians) to bring them up to normal may not be so bad, even if combined with caffeine. But this study might be a warning for bodybuilders who may already have plenty of creatine from their omnivorous, animal-protein-rich diet and may supplement creatine and consume caffeine on top of that.

 

--Dean

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Any significant updates on the original thread by MR (and the creatine offshoot)? 

Edited by mccoy

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Re. Creatiine: I listened to a pretty good podcast by Chris Masterjohn and Alex leaf:

Creatine: Far More Than a Performance Enhancer

It underlines the metabolic advantages of creatine supplementation beyond the increase in strenght and muscle hydration/size. Apparently good for the sight, the hearing and the gastric digestion as well.

It convinced me to try the saturation protocol described in detail in the podcast. 30% of the people are refractory to the beneficial effects though, even though it's not clear if they are muscularly refractory or metabolically refractory as well.

The saturation protocol implies dosages of 3 to 5 grams per day of creatine monohydrate for a duration of about 4 weeks. After the muscle saturation is reached, the quantity may go back to daily usage (about 2 g/d) . In such doses there should no be detrimental interactions with caffeine.

Of course, we may choose to avoid or check caffeine if we choose the creatine gamble.

 

Edited by mccoy

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