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All,

 

So (dark) chocolate and other cacao-derived products (i.e. cacao beans, nibs, cocoa powder) have a lot of beneficial phytochemicals (polyphenols, flavonols, etc). These have been shown to be beneficial for both the cardiovascular system and the brain - this is pretty well established, so I'm not including references (I know you are disappointed...). Alright - maybe one reference [2] - a review of CVD benefits of chocolate. Later... - here is another [4], on brain benefits of chocolate.

 

But as we've discussed recently, these chocolate products have some things we'd rather avoid ingesting, including saturated fat (except for cocoa powder), and potential heavy metal contaminants, especially cadmium.

 

What other food items have this same "take the good with the bad" quality? Two spring to mind - coffee and tea. But in these two cases, we don't take the good with the bad. We process them in such a way as to get the good without the bad.

 

I was reminded of this today when responding to this post on the potential heavy metal contamination associated with consuming matcha green tea - where the tradition is to eat the tea leaves. By brewing green tea, and discarding the leaves, we retain the beneficial tea polyphenols but eliminate the heavy metals.

 

Similarly, in this discussion we talked about getting the benefits of coffee beans by brewing and then filtering them, with paper (or possibly? metal) filters to eliminates the cholesterol-raising diterpenes cafestol and kahweol that the beans naturally contain, while retaining the health-promoting phytochemicals in coffee.

 

So why don't we do the same thing for chocolate? Namely, why don't we grind, brew and filter the coffee beans to extract that beneficial polyphenols into the water, while leaving (most?) of the heavy metals and saturated fat in the solid "chocolate grounds"?

 

Well, I can think of one possible reason we don't do this - we like the taste and mouth feel of actually eating the chocolate. But putting that (admittedly big deterrent for some) aside, is there reason to believe this strategy wouldn't work to get most of the health benefits of chocolate without the potential downsides of heavy metals and saturated fat, not to mention the extra calories?

 

First, regarding eliminating the 'bad stuff' by brewing and filtering chocolate.

 

For heavy metals, it would seem no different from tea or coffee. Since the heavy metals appear to remain locked in the plant matrix of the discarded solids (coffee grounds or tea leaves), I see no good reason to think it would be different with the heavy metal contaminants in cacao beans. Anyone think otherwise?

 

Regarding the other 'bad stuff' in cacao / chocolate - the saturated fat. Its hard to find nutrition information on coffee beans (as eaten) - without any chocolate coating... CRON-O-Meter comes up empty. But I did find two references to the calories in coffee beans themselves. The first lists 100g of coffee beans as having 406kcal, 10.2g of fat, with 4.8g of it saturated. Not too far from raw cacao beans in fact. The second also listed 10g of fat per 100g of beans, with somewhat fewer calories (300kcal).

 

Either way, these illustrate that coffee beans themselves contain a lot of fat, but as we all know, brewed coffee has virtually none. So clearly fat doesn't get extracted to the liquid as a result of brewing and filtering coffee beans, so I would expect the same for cacao beans - right?

 

What about the other side of the equation - should we expect the 'good stuff' in chocolate to get extracted to the water when brewed and filtered, like it does for tea and coffee?

 

Again - I don't see why not. As I understand it, based on information from [2] (a very good source of info about polyphenols in cacao, BTW) and [3] (also a good source), the taxonomy of beneficial phytochemicals (with special emphasis on those in cacao) goes something like this:

  • All Phytochemicals
    • All Polyphenols
      • All Flavonoids
        • All proanthocyanidin?
          • All Flavanols
            • catechins - in either monomeric or multimeric (procyanidin) forms
            • epicatechins - in either monomeric or multimeric (procyanidin) forms
          • ...
        • ...
      • See here for list
    • ...
  • ..
Note: I'm not exactly sure about this taxonomy, especially where proanthocyanidin fits in - the literature is very confusing.

 

But the important thing is that the main phytochemicals in cacao are catechins and epicatechins, which should be familiar to people. They are (among) the healthy phytochemicals found in green tea. So clearly if they are water-soluble in green tea, they should be water soluble in ground cacao beans as well, it would seem.

 

So, as a result of all this, it seems logical to me that grinding, brewing and filtering cacao beans should get rid of the bad stuff (heavy metals, saturated fat, and calories) and extract the good stuff (the polyphenols) into the resulting watery brew. Note - I should have said this earlier, we aren't talking about brewing hot chocolate here - where the cocoa powder is mixed in with the liquid and consumed. We're brewing ground cacao beans, filtering (with a paper filter) to separate the liquid from the grounds, then discarding the grounds and drinking the coffee-like chocolate brew.

 

But what to do with the beans before grinding them? In particular, should they be roasted, like coffee beans are? Perhaps to reduce bitterness, but if one wants to maximize polyphenols, it seems from [1] that grinding raw beans would be best.

 

You won't be surprised to learn that this isn't a novel idea. In fact, there are several commercially-available products for brewing cacao as you would coffee. The two most popular are Crio Bru and Choffy (cute name!). They are both a bit more expensive than coffee, although pretty close to the price of premium coffee beans. Not surprisingly, they are both roasted, presumably to improve flavor and reduce bitterness. They recommend using a french press to brew, which I have, but I wonder if the Aeropress will work as well (Choffy's website says yes! and gives instructions). Here is a good overview from a "chocolate geek" about brewing chocolate, including a review of Crio Bru and Choffy products. It sounds very promising, and not hard to do. You can also buy ground brewing chocolate from his website as well.

 

In the long-run if I like it and the above reasoning isn't shot down..., I'll probably grind my own raw beans or lightly roast the beans myself before grinding (I've roasted coffee beans before using an air popcorn popper - its a piece of cake). But for now, I've ordered one of the Crio Bru varieties from Amazon (Choffy was more expensive and not available via Amazon Prime). It should arrive in a couple days and I'll let you know what it is like relative to coffee.

 

In the meantime, I'm very curious about what other people think of this idea. I can certainly imagine people balking at the diminished enjoyment of drinking coffee-like chocolate rather than eating the 'real thing' or even drinking cocoa, but I'm most interested about people's thoughts on the health angle. Also if you've ever actually tried brewed chocolate, I'd love to hear what you think!

 

--Dean

 

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

[1] Food Chem. 2015 May 1;174:256-62. doi: 10.1016/j.foodchem.2014.11.019. Epub 2014

Nov 8.

 

Flavanols, proanthocyanidins and antioxidant activity changes during cocoa

(Theobroma cacao L.) roasting as affected by temperature and time of processing.

 

Ioannone F(1), Di Mattia CD(2), De Gregorio M(2), Sergi M(2), Serafini M(3),

Sacchetti G(4).

 

The effect of roasting on the content of flavanols and proanthocyanidins and on

the antioxidant activity of cocoa beans was investigated. Cocoa beans were

roasted at three temperatures (125, 135 and 145 °C), for different times, to

reach moisture contents of about 2 g 100 g(-1). Flavanols and proanthocyanidins

were determined, and the antioxidant activity was tested by total phenolic index

(TPI), ferric reducing antioxidant power (FRAP) and total radical trapping

antioxidant parameter (TRAP) methods. The rates of flavanol and total

proanthocyanidin loss increased with roasting temperatures. Moisture content of

the roasted beans being equal, high temperature-short time processes minimised

proanthocyanidins loss. Moisture content being equal, the average roasting

temperature (135 °C) determined the highest TPI and FRAP values and the highest

temperature (145 °C) determined the lowest TPI values. Moisture content being

equal, low temperature-long time roasting processes maximised the chain-breaking

activity, as determined by the TRAP method.

 

Copyright © 2014 Elsevier Ltd. All rights reserved.

 

PMID: 25529678

 

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

[2] Nutrients. 2014 Feb 21;6(2):844-80. doi: 10.3390/nu6020844.

Cocoa polyphenols and inflammatory markers of cardiovascular disease.

 

Khan N(1), Khymenets O(2), Urpí-Sardà M(3), Tulipani S(4), Garcia-Aloy M(5),

 

Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942736/

Monagas M(6), Mora-Cubillos X(7), Llorach R(8), Andres-Lacueva C(9).

 

Epidemiological studies have demonstrated the beneficial effect of plant-derived

food intake in reducing the risk of cardiovascular disease (CVD). The potential

bioactivity of cocoa and its polyphenolic components in modulating cardiovascular

health is now being studied worldwide and continues to grow at a rapid pace. In

fact, the high polyphenol content of cocoa is of particular interest from the

nutritional and pharmacological viewpoints. Cocoa polyphenols are shown to

possess a range of cardiovascular-protective properties, and can play a

meaningful role through modulating different inflammatory markers involved in

atherosclerosis. Accumulated evidence on related anti-inflammatory effects of

cocoa polyphenols is summarized in the present review.

 

PMCID: PMC3942736

PMID: 24566441

 

[3] http://www.medscape.com/viewarticle/590371

 

Quoting from it:

 

 

 

 

 

The main flavanols present in the cocoa powder are catechins and epicatechins in either monomeric or multimeric (procyanidin) forms.

--------

[4] http://newsroom.cumc.columbia.edu/blog/2014/10/26/flavanols-memory-decline/

 

"Dietary cocoa flavanols—naturally occurring bioactives found in cocoa—reversed age-related memory decline in healthy older adults, according to a study led by Columbia University Medical Center (CUMC) scientists. The study, published today in the advance online issue of Nature Neuroscience, provides the first direct evidence that one component of age-related memory decline in humans is caused by changes in a specific region of the brain and that this form of memory decline can be improved by a dietary intervention."

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I usually have 16 grams of coffee beans (Lido 2 grinder) through a pourover at ~250g of water.  Today, I tried 4g of ground cacao nibs underneath 12g coffee bean (roasted last week) with a 2m30s brew time @ 208F.  Pretty awesome taste, although I could use more coffee bean and more cacao flavor (and maybe a touch of vanilla bean powder and/or ceylon cinnamon.)  Great suggestion.

 

I don't find the bitterness much of an issue (this was actually a pretty sweet cup of coffee.)  I usually drink my coffee black and fairly strong, and enjoy this with a side of unsweetened raw nibs / 88%-100% extra dark chocolate.

 

I believe the common "brewing chocolates" contain more shell (if not mostly roasted husk), which might be sub-optimal for the purposes of maintaining a very high nutrient / polyphenol : anti-nutrient / toxin / heavy metal ratio.  I believe cacao is also fairly rich in oxalates / phytic acid, which might not have been mentioned.  I'm curious if the ideal steep time is similar to coffee and how brewing compares with eating the cacao in terms of polyphenol / metal exposure.  The bullet proof coffee guy also sells brewing chocolate ("cacao tea"), although he recommends drinking it with lots of butter added, of course.

 

After drinking this coffee, I couldn't help but think "You know what would go great with this coffee?  Some dark chocolate and some nibs."  This might only serve to further increase my cacao intake.

Edited by sirtuin

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Sirtuin,

 

Thanks for trying adding cacao nibs to your coffee brewing strategy. That sounds very promising. I too will probably do a mix of coffee, cacao and maybe tea too, once my beans / Crio Bru arrives.

 

After drinking this coffee, I couldn't help but think "You know what would go great with this coffee?  Some dark chocolate and some nibs."  This might only serve to further increase my cacao intake.

 

I can imagine that reaction as well!  :)xyz

 

--Dean

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Thanks for the idea Dean and I may experiment with it but aren't you concerned with the possible Parkinson's link for heavy chocolate consumers?

 

http://www.confectionerynews.com/Regulation-Safety/Chocolate-over-consumption-may-be-linked-to-Parkinson-s-Disease-review

 

Michael Rae has a archive post or two on a previous study too. These days I eat a maximum of one bar a month (Trader Joes Maltitol 50% cacao, 4 cals a gram).  

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Thanks for the idea Dean and I may experiment with it but aren't you concerned with the possible Parkinson's link for heavy chocolate consumers?

 

http://www.confectionerynews.com/Regulation-Safety/Chocolate-over-consumption-may-be-linked-to-Parkinson-s-Disease-review

 

Michael Rae has a archive post or two on a previous study too. These days I eat a maximum of one bar a month (Trader Joes Maltitol 50% cacao, 4 cals a gram).  

It mentions a risk here as low as 0.63mg/day of beta-PEA where 100g of chocolate maxes out around 0.83 mg/day.  My upper dose is usually around 20g of lindt 85%, or 12g in a day of 88%, and ~ 3-6 grams with 100% cacao.  At 20g + 12g + 6g if I went crazy on chocolate that day, I would be hitting 38 grams (still under this threshold.)  This doesn't seem like a large risk factor for me, unless I'm adding this up wrong.

Edited by sirtuin

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Thanks for the idea Dean and I may experiment with it but aren't you concerned with the possible Parkinson's link for heavy chocolate consumers?

 

http://www.confectionerynews.com/Regulation-Safety/Chocolate-over-consumption-may-be-linked-to-Parkinson-s-Disease-review

 

Michael Rae has a archive post or two on a previous study too.

 

Martin,

 

Thanks for bringing this to my attention again. Here is Michael Rae's somewhat rambling post on the topic of chocolate and Parkinson's disease (no offense Michael - it is a somewhat murky topic. I'll try to make some sense of it, like you requested in that post... )

 

The link Martin posted points to this review study [1] that postulates a mechanism by which β-phenethylamine (β-PEA), a chemical found in chocolate, wine and cheese, might be toxic to the dopamine-sensitive neurons whose death is implicated in Parkinson's disease.

 

That review cites [2], which talks about how administering high doses of β-PEA via injection to mice appears to produce Parkinson's-like behavioral symptoms (e.g. impaired swimming performance), and reduction in dopamine levels in the part of the brain associated with Parkinson's, although no overt cell death was observed in that area, as is observed in Parkinson's. Nevertheless, that does sound troubling for chocolate.

 

Note though, [2] also reports that administering high dose of β-PEA to rats via oral ingestion (rather than injection) did not result in the same negative, Parkinson's-like consequences. So injecting β-PEA into mice appeared to produce Parkinson's-like effects, but ingestion (by rats) of a similar dose did not. Ignoring any difference between mice and rats (hereafter equated and referred to as 'rodents' in this post), this suggests the digestion process breaks down the β-PEA, or otherwise prevents it from making it into the bloodstream. To quote [2]:

 

However, per-oral administration of higher doses of PEA (75-125 mg/kg; 7 days) failed to cause such overt neurochemical effects in rats, which suggested safe consumption of food items rich in this trace amine by normal population

 

Now let's put that together with [3] a study of chocolate, β-PEA and Parkinson's in humans. It investigated whether ingesting chocolate had any effect on motor function in Parkinson's patients, actually hypothesizing that β-PEA might improve motor function. Unfortunately, it didn't. But it didn't make motor function worse either. Furthermore, and more importantly relative to [1] and [2], it found:

 

 β-phenylethylamine blood levels were unaltered.  

 

So like with the rodents, when people eat β-PEA, in the form of nearly a half pound of 80% cacao dark chocolate, there is no rise in their blood level of β-PEA. If levels don't rise in the blood, then presumably, the β-PEA can't get to the brain to mess up Parkinson's-associated striatal neurons.

 

In short, it doesn't appear to me like there is any evidence that whatever β-PEA there is in chocolate makes it into the bloodstream, to say nothing of the brain. Note - β-PEA is an endogenously-produced chemical, so we've already got it in our brain naturally in trace amounts.

 

But let's assume this is wrong, and that these studies are mistaken, and that orally-ingested β-PEA can get to the brain. How much β-PEA is there really in cacao and chocolate products?

 

Study [4] tested a range of chocolate liquor and chocolate bars, and found between 0.44 and 8 micrograms per gram of chocolate product. Here are the relevant tables from [4] (see last column of each):

 

NJ9riVO.png

 

fcV0ECW.png

 

Let's go with a number towards the upper part of the β-PEA in any of these samples, say 6 ug per gram of chocolate. A ug (microgram, also known as mcg) is a millionth of a gram. So that equates to a level of 6 PPM of β-PEA in chocolate. Conveniently, study [5] found similar levels - almost all the samples were below 6 PPM. Here is the table from [5]:

 

4Sc1ebW.png

 

So from [3] and [4], if you ate in the ballpark of a million grams of chocolate, you'd get about 6g dose of β-PEA. 

 

Now if I'm interpreting [2] right, they were administering β-PEA (either intravenously which had an effect, or orally with no effect) at a level of about 75-125 mg/kg, where, presumably, the 'kg' refers to kg body weight of the rodents. 

 

If we do a naive scaling to a 65kg human,it would require a person to ingest approximately 6500 mg, or 6.5g of β-PEA per day to get to the bloodstream level of β-PEA these rodents were getting (when injected with the stuff). That 6.5g is conveniently close to the 6g of β-PEA in a million grams of chocolate. So to get the equivalent dose the rodents were receiving intravenously in this study, a person would have to eat a ton of chocolate (Actually 1.2 tons, since 1 US Ton = 907,184 grams), per day assuming (against the evidence) that all the orally ingested β-PEA actually gets into the blood.

 

I fear I'm doing something wrong here, and will be very embarrassed when Michael or someone else points out my mistake(s). I'm particularly worried since it appears from Michael's post that he gave up trying to make sense of the available data on chocolate and Parkinson's disease...

 

If I'm wrong, they'll definitely be egg on my face. But fortunately, I'll correct this post and cover my tracks by using my moderator superpowers to delete the post of whoever corrects me  :ph34r: - so posterity will never see my faux pas. Just kidding...  :)xyz

 

But if my interpretations are correct, you'd have to eat over a ton (literally) of chocolate per day to get doses that negatively affected rodents, but only when injected and not when ingested, as is typically the case with chocolate products. :)xyz

 

In short, I very well could be wrong, but it doesn't look to me like there is much reason to worry about chocolate and Parkinson's disease...

 

--Dean

 

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

[1] Neurosci Bull. 2013 Oct;29(5):655-60. doi: 10.1007/s12264-013-1330-2. Epub 2013

Apr 10.

 

Contribution of β-phenethylamine, a component of chocolate and wine, to

dopaminergic neurodegeneration: implications for the pathogenesis of Parkinson's

disease.

 

Borah A(1), Paul R, Mazumder MK, Bhattacharjee N.

Author information:

(1)Department of Life Science and Bioinformatics, Assam University, Silchar,

788011, Assam, India, anupomborah@gmail.com.

 

While the cause of dopaminergic neuronal cell death in Parkinson's disease (PD)

is not yet understood, many endogenous molecules have been implicated in its

pathogenesis. β-phenethylamine (β-PEA), a component of various food items

including chocolate and wine, is an endogenous molecule produced from

phenylalanine in the brain. It has been reported recently that long-term

administration of β-PEA in rodents causes neurochemical and behavioral

alterations similar to that produced by parkinsonian neurotoxins. The toxicity of

β-PEA has been linked to the production of hydroxyl radical ((·)OH) and the

generation of oxidative stress in dopaminergic areas of the brain, and this may

be mediated by inhibition of mitochondrial complex-I. Another significant

observation is that administration of β-PEA to rodents reduces striatal dopamine

content and induces movement disorders similar to those of parkinsonian rodents.

However, no reports are available on the extent of dopaminergic neuronal cell

death after administration of β-PEA. Based on the literature, we set out to

establish β-PEA as an endogenous molecule that potentially contributes to the

progressive development of PD. The sequence of molecular events that could be

responsible for dopaminergic neuronal cell death in PD by consumption of

β-PEA-containing foods is proposed here. Thus, long-term over-consumption of food

items containing β-PEA could be a neurological risk factor having significant

pathological consequences.

 

PMID: 23575894

 

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

[2] Neurochem Int. 2010 Nov;57(6):637-46. doi: 10.1016/j.neuint.2010.07.013. Epub

2010 Aug 4.

 

2-Phenylethylamine, a constituent of chocolate and wine, causes mitochondrial

complex-I inhibition, generation of hydroxyl radicals and depletion of striatal

biogenic amines leading to psycho-motor dysfunctions in Balb/c mice.

 

Sengupta T(1), Mohanakumar KP.

 

Author information:

(1)Laboratory of Clinical and Experimental Neurosciences, Division of Cell

Biology and Physiology, Indian Institute of Chemical Biology (CSIR, Govt. of

India), 4 Raja S C Mullick Road, Jadavpur, Kolkata 700032, India.

 

Behavioral and neurochemical effects of chronic administration of high doses of

2-phenylethylamine (PEA; 25-75 mg/kg, i.p. for up to 7 days) have been

investigated in Balb/c mice. Depression and anxiety, as demonstrated respectively

by increased floating time in forced swim test, and reduction in number of

entries and the time spent in the open arms in an elevated plus maze were

observed in these animals. General motor disabilities in terms of akinesia,

catalepsy and decreased swimming ability were also observed in these animals.

Acute and sub-acute administration of PEA caused significant, dose-dependent

depletion of striatal dopamine, and its metabolites levels. PEA caused

dose-dependent generation of hydroxyl radicals in vitro in Fenton's reaction in

test tubes, in isolated mitochondrial fraction, and in vivo in the striatum of

mice. A significant inhibition of NADH-ubiquinone oxidoreductase (complex-I; EC:

1.6.5.3) activity suggests the inhibition in oxidative phosphorylation in the

mitochondria resulting in hydroxyl radical generation. Nissl staining and TH

immnunohistochemistry in brain sections failed to show any morphological

aberrations in dopaminergic neurons or nerve terminals. Long-term

over-consumption of PEA containing food items could be a neurological risk factor

having significant pathological relevance to disease conditions such as

depression or motor dysfunction. However, per-oral administration of higher doses

of PEA (75-125 mg/kg; 7 days) failed to cause such overt neurochemical effects in

rats, which suggested safe consumption of food items rich in this trace amine by

normal population.

 

Copyright © 2010 Elsevier Ltd. All rights reserved.

 

PMID: 20691235

 

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

[3] J Neurol. 2012 Nov;259(11):2447-51. doi: 10.1007/s00415-012-6527-1. Epub 2012 May

15.

 

Comparison of chocolate to cacao-free white chocolate in Parkinson's disease: a

single-dose, investigator-blinded, placebo-controlled, crossover trial.

 

Wolz M(1), Schleiffer C, Klingelhöfer L, Schneider C, Proft F, Schwanebeck U,

Reichmann H, Riederer P, Storch A.

 

Author information:

(1)Division of Neurodegenerative Diseases, Department of Neurology, Dresden

University of Technology, Fetscherstraße 74, 01307, Dresden, Germany.

 

A previous questionnaire study suggests an increased chocolate consumption in

Parkinson's disease (PD). The cacao ingredient contains caffeine analogues and

biogenic amines, such as β-phenylethylamine, with assumed antiparkinsonian

effects. We thus tested the effects of 200 g of chocolate containing 80 % of

cacao on UPDRS motor score after 1 and 3 h in 26 subjects with moderate

non-fluctuating PD in a mono-center, single-dose, investigator-blinded crossover

study using cacao-free white chocolate as placebo comparator. At 1 h after

chocolate intake, mean UPDRS motor scores were mildly decreased compared to

baseline in both treatments with significant results only for dark chocolate

[-1.3 (95 % CI 0.18-2.52, RMANOVA F = 4.783, p = 0.013¸ Bonferroni p = 0.021 for

1 h values)]. A 2 × 2-cross-over analysis revealed no significant differences

between both treatments [-0.54 ± 0.47 (95 % CI -1.50 to 0.42), p = 0.258].

Similar results were obtained at 3 h after intake. β-phenylethylamine blood

levels were unaltered. Together, chocolate did not show significant improvement

over white cacao-free chocolate in PD motor function.

 

PMID: 22584952

 

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

[4] High-performance liquid chromatographic determination of four biogenic amines in chocolate

W. Jeffrey Hurst and    Paul B. Toomey  
Analyst, 1981,106, 394-402
DOI: 10.1039/AN9810600394

 

Full Text: http://pubs.rsc.org/en/content/articlelanding/1981/an/an9810600394#!divAbstract

 

Some biogenic amines occur in a wide variety of foods including cheese, fish, bakery products, milk products and chocolate. This study was undertaken to analyse and quantify four of the biogenic amines thought to occur in chocolate. Tyramine, tryptamine, 2-phenylethylamine and serotonin (5-hydroxytryptamine) were chosen as the amines of interest. Two high-performance liquid chromatographic (HPLC) systems were used for the final analysis of amine extracts. Both systems employed dual detection, with the first using ultraviolet absorbance at 254 nm and the formation of a post-column o-phthaldehyde derivative. The second method used ultraviolet absorbance at 254 nm and the natural fluorescence of the four amines. Thin-layer chromatography (TLC) was performed on all of the extracts to provide further confirmation. All four amines were detected and quantified at varying levels in extracts of several kinds of chocolate and chocolate liquors.

 

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

[5] Food Chemistry

Volume 6, Issue 4, Pages 281-288, June, 1981
 
Changes in the levels of 2-phenylethylamine in cheese and chocolate during processing and storage
 
M.J. Saxby, J.P. Chaytor, R.G. Reid
 
 
Abstract
 
Amines from cheese and chocolate were extracted with solvent and separated from non-basic material on an ion-exchange column. The amines were reacted with trifluoroacetic anhydride after the addition of aminotetrahydronaphthalene as an internal standard. The derivatives were analysed on a SCOT column by gas chromatography. The levels of phenylethylamine increased in cocoa beans during fermentation and roasting. Some samples of cheese contained phenylethylamine. whereas others prepared aseptically did not.

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Dean wrote:

In short, it doesn't look to me like there is much reason to worry about chocolate and Parkinson's disease...

Dean,

 

I like how you provide a summary at the end of your post. It helps, even though I did read the entire post.

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I like how you provide a summary at the end of your post. It helps, even though I did read the entire post.

 

Thanks Greg. I aim to please, and I realize not everyone has the time or the inclination to read all the details. Hopefully in this case, the details are sound. Otherwise there could be a big retraction in order...

 

--Dean

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Thanks Dean for your thorough response to my link. I looked it up quickly and hadn't noticed the PEA was injected and that there was another study showing oral ingestion of dark chocolate didn't raise levels of PEA.

 

However even if we throw the rodent data and the PEA mechanism out we still have the earlier (unfortunately unpublished) Goldman study showing those who ate 2-3 bars a week (and many of those of course and possibly ironically were much lower in cacao than the stuff health conscious people like ourselves are likely to eat - that dose might be equivalent to only a single bar a week of the very dark stuff) were more than three times at risk for Parkinson's. 

 

http://www.yourlawyer.com/articles/title/pesticide-link-to-parkinson8217s-probed

 

(near bottom of page)

 

And the risk is not tiny to start with; prevalence is 2% for the over 80s:

 

http://www.ncbi.nlm.nih.gov/pubmed/24976103

 

My philosophy is there's plenty of other things to eat.

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Martin,

Thanks Dean for your thorough response to my link. I looked it up quickly and hadn't noticed the PEA was injected and that there was another study showing oral ingestion of dark chocolate didn't raise levels of PEA.

 

However even if we throw the rodent data and the PEA mechanism out we still have the earlier (unfortunately unpublished) Goldman study showing those who ate 2-3 bars a week (and many of those of course and possibly ironically were much lower in cacao than the stuff health conscious people like ourselves are likely to eat - that dose might be equivalent to only a single bar a week of the very dark stuff) were more than three times at risk for Parkinson's.

 

http://www.yourlawyer.com/articles/title/pesticide-link-to-parkinson8217s-probed (near bottom of page)

Here we go again...

 

First off, Parkinson's Disease (PD) is believed to be a complex interplay between genes and environment [2]. In fact, on the webpage you reference, Samuel Goldman, the author of the chocolate study you point to [1] and well know PD researcher, says as much:

 

 

“We don’t think any one compound causes Parkinson’s disease because then we would expect to see more clusters of cases,” said Goldman. “So it has got to be a whole lifetime of mild insults that set off a degenerative cascade in the brain.”

Study [1] is referenced in the Goldman's CV and one of the other authors, but nowhere else on the internet. So we don't even have an abstract to go on, only the information reported by this "highly-reputable" health-oriented website YourLawyer.com... But let's put that aside and look at the science.

 

It is a study from 2002. You'd think that in the intervening 13 years if chocolate really was associated with PD, these authors, or the thousands of others involved in PD research, would have noticed by now and published about it. But despite remaining a leader in the field, with a continuous publication record through this year, Dr. Goldman has never published anything further (or anything at all, since this study [1] apparently was never actually published, and isn't indexed in PubMed) about an association between chocolate and PD. In fact, this thorough 2015 review [3] of the evidence for dietary factors associated with PD, mentions chocolate only once, in a positive light, due to its caffeine content (~80mg /2oz serving, vs. ~150mg / 8oz coffee) which has been strongly linked to a decreased risk of PD. [Note: Milk on the other hand, doesn't appear to be so lucky - [11] found a 2.3x increased rate of PD in middle-aged milk drinkers, although the recent review [3] doesn't say much about milk/cheese except in the context of saturated fat, which increases risk of PD).

 

But let's focus back on the available information we have for Martin's study [1] that alleges a possible link between chocolate and PD. Here is a quote from the article:

 

 

Goldman, who was lead author of this study, asked 72 pairs of twins in which one had Parkinson’s and the other did not about their dietary habits in the 10 years prior to one of them developing the disease. He found those who ate [more accurately - retrospectively reported to have eaten - DP] a lot of chocolate — two to three candy bars per week — had more than a three-fold increased risk of having Parkinson’s than those who ate less. He also found a smaller link with wine and with a measure of total IQ consumption. “The population is fairly small and the data is extremely retrospective,” he said. “But in basic science research there’s probably a reason to suspect these compounds [isoquinloines].” Brey noted that dietary histories are often unreliable. “People don’t remember what they’ve eaten years ago and if you had bad information you are going to have erroneous results.

So this is a very weak, retrospective study with a very small number of subjects, that experts were criticizing at the time it was (almost) published, and that nobody has found reason to follow up on in the 13 years since. Doesn't seem like a very strong indictment against chocolate (or wine, which also contains isoquinloines).

 

But in case you're not convinced, let's continue to beat this mortally-wounded horse.

 

Isoquinloines are endogenous compounds generated in the brain by a very complicated process, and they do seem to be associated with Parkinson's Disease [4]. They are also found in some foods [6], which mentions "cheese, milk, red wine, bananas, etc". While no mention is made of chocolate as a dietary source Isoquinloines in [6], its clear from other sources (e.g. [7]), that chocolate does indeed contain a compound called salsolinol (SAL) which is in the isoquinloine family. SAL, and the other isoquinloines, increase dopamine in the brain, and according to [7]:

 

 

...salsolinol seems to be one of the main psychoactive compounds present in cocoa and chocolate and might be included in chocolate addiction.

[Note - while this isn't part of the main story, even if PD patients eat more chocolate, there might be another, more plausible explanation than "chocolate causes PD". PD is defined as the degeneration of dopamine producing neurons in the brain. Perhaps eating chocolate and other dopamine-increasing foods is a way for PD patients, or those at an early stage of developing PD without overt symptoms, to compensate for a lack of pleasure-inducing dopamine in their brain - i.e. self-medicating. I acknowledge that Michael Rae rejects this "self-medicating" hypothesis for the possible elevation of dopamine-increasing foods like chocolate in the diets of PD patients, based on evidence that consumption of such dopaminergic foods don't improve the motor symptoms of PD patients. But just because a self-treatment doesn't work doesn't mean we don't engage in it in hopes that it will. Just ask anyone who has eaten a whole pint of ice cream after a bad day whether it works to really make them feel better. But there is no denying he/she ate the ice cream in the mistaken and perhaps unconscious belief that it would make them feel better in some way.]

 

Back to our story. So chocolate contains SAL. Is SAL harmful? Study [8] found that SAL appears elevated in cerebrospinal fluid of PD patients, and in vitro at least, high concentrations of SAL causes dopamine neurons to die via apoptosis. That doesn't sound good...

 

So understandably, several recent studies [9][10] have investigated the link between SAL and PD.

 

Study [9] was interesting. First, because it involved bananas, another of my favorites! It turns out not just chocolate that contains SAL, but bananas as well. The study fed one banana to human subjects, and fed 3g of banana (or a dose of pure SAL via the stomach) to rats, to see what that would do to SAL levels in the blood (in both species), and in the brain (rats only :)xyz). So what did they find?

 

In humans, eating a banana-containing breakfast did indeed increase both SAL and dopamine (DA) levels in the blood, which peaked about about 1 - 1.5 hours. Similar rises were observed in the rats after ingestion of banana (or pure SAL, without the bump in plasma dopamine). But, importantly, [9] found:

 

 

Despite the increases seen in plasma SAL or DA levels after banana ingestion, those levels in the brain were not changed either in NAC or STR [nucleus accumbens or striatum - the two areas of the brain that degenerate in PD] at any time points examined.

<snip>

Our data indicated no correlation between the plasma and brain SAL levels in rats (Fig. 4B, Table 1). It is well recognized that most catecholamines in plasma are not incorporated into the central nervous system (CNS) due to inability to cross the blood–brain barrier (BBB). The SAL detected in the brain is likely to be derived from in situ synthesis (Origitano et al., 1981), although sodium-independent organic cation transporter (OCT-2) has been recently recognized as a possible active transporter of SAL (Taubert et al., 2007). Our data indicated no changes in SAL concentrations in rat brains despite significant increases of plasma SAL levels after banana administration, supporting the idea that peripheral SAL may not significantly contribute to the brain SAL concentration.

So, for those of you following along, dietary salsolinol (SAL), the potentially troublesome isoquinloine in chocolate (and bananas) that Martin's study was worried about as a potential cause of PD, doesn't appear to make it from the blood to the brain.

 

Finally, [10] appears to put the final nail in the coffin of the poor horse that we started beating many studies ago (sorry to mixed metaphor). Less than a year ago, it found that modest levels of SAL may actually be protective against PD-like neurodegeneration:

 

 

Summarizing, the present studies exclude possibility that salsolinol under physiological conditions could be an endogenous factor involved in the neurogenerative processes; conversely, it can exert a protective action on nerve cells in the brain. These findings may have important implications for the development of the new strategies to treat or prevent neural degeneration.

In other words, even the endogenous SAL synthesized naturally in the brain may be neuroprotective, rather than neurotoxic at typical physiological levels. So even if (against the evidence) a small amount of SAL seeps into the brain from eating chocolate (or bananas), it is more likely to prevent, rather than cause, PD.

 

RIP to the horse that said "chocolate may cause Parkinson's disease because it contains the isoquinloine salsolinol".

My philosophy is there's plenty of other things to eat.

Martin, you can point to just about any food and identify potential downsides. My philosophy is to eat a wide variety of foods for which there is evidence of beneficial health effects, and eat them in relatively small quantities to minimize the risk of excessive exposure to any one harmful substance. Chocolate is one such 'functional' food.

 

Speaking of which, its time to go try the brewing chocolate that was just delivered (just in time for my b-day) via Amazon Prime!

 

--Dean

 

 

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

[1] Goldman SM, Kusumi M, Aston DA, Langston JW, Tanner CM. Dietary intake of isoquinoline derivatives (IQs) and PD: A study in twins. Neurology April 2002; 58 (Suppl 3): A409.

 

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

[2] Ann Neurol. 2003;53 Suppl 3:S16-23; discussion S23-5.

Genetic and environmental factors in the cause of Parkinson's disease.

 

Warner TT(1), Schapira AH.

 

Author information:

(1)Department of Clinical Neurosciences, Royal Free and University College

Medical School, London NW3 2PF, United Kingdom.

 

Despite being the subject of intense study, the pathogenesis of Parkinson's

disease still remains unclear. In recent years, however, there has been

increasing evidence to support a role for genetic factors in its cause. This has

come from twin and family studies, the mapping and cloning of PARK genes that are

associated with the development of PD, and analysis of potential susceptibility

genes. There is also evidence indicating that environmental factors may play a

role in the disease process. It is likely that for most cases, there is a complex

interplay between these genetic and environmental influences in the causation of

Parkinson's disease. This article reviews the evidence in support of genetic and

environmental factors in the cause of PD.

 

PMID: 12666095

 

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

[3] BioMed Research International, vol. 2015, Article ID 672838, 16 pages, 2015. doi:10.1155/2015/672838

 

“Dietary Factors in the Etiology of Parkinson’s Disease,”

 

Zeynep S. Agim and Jason R. Cannon,

 

Free full text: http://www.hindawi.com/journals/bmri/2015/672838/

 

Abstract

 

Parkinson’s disease (PD) is the second most common neurodegenerative disorder. The majority of cases do not arise from purely genetic factors, implicating an important role of environmental factors in disease pathogenesis. Well-established environmental toxins important in PD include pesticides, herbicides, and heavy metals. However, many toxicants linked to PD and used in animal models are rarely encountered. In this context, other factors such as dietary components may represent daily exposures and have gained attention as disease modifiers. Several in vitro, in vivo, and human epidemiological studies have found a variety of dietary factors that modify PD risk. Here, we critically review findings on association between dietary factors, including vitamins, flavonoids, calorie intake, caffeine, alcohol, and metals consumed via food and fatty acids and PD. We have also discussed key data on heterocyclic amines that are produced in high-temperature cooked meat, which is a new emerging field in the assessment of dietary factors in neurological diseases. While more research is clearly needed, significant evidence exists that specific dietary factors can modify PD risk.

 

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

[4] Biochem Pharmacol. 1998 Oct 15;56(8):921-33.

Isoquinoline derivatives as endogenous neurotoxins in the aetiology of

Parkinson's disease.

 

McNaught KS(1), Carrupt PA, Altomare C, Cellamare S, Carotti A, Testa B, Jenner

P, Marsden CD.

 

The cause of neurodegeneration in Parkinson's disease (PD) remains unknown.

However, isoquinoline derivatives structurally related to the selective

dopaminergic toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its

active metabolite, 1-methyl-4-phenylpyridinim (MPP+), have emerged as candidate

endogenous neurotoxins causing nigral cell death in Parkinson's disease.

Isoquinoline derivatives are widely distributed in the environment, being present

in many plants and foodstuffs, and readily cross the blood-brain barrier. These

compounds occur naturally in human brain where they are synthesized by

non-enzymatic condensation of biogenic amines (e.g. catecholamines and

phenylethylamine) with aldehydes, and are metabolized by cytochrome P450s and

N-methyltransferases. In addition, isoquinoline derivatives are oxidized by

monoamine oxidases to produce isoquinolinium cations with the concomitant

generation of reactive oxygen species. Neutral and quaternary isoquinoline

derivatives accumulate in dopaminergic nerve terminals via the dopamine re-uptake

system, for which they have moderate to poor affinity as substrates. Several

isoquinoline derivatives are selective and more potent inhibitors of NADH

ubiquinone reductase (complex I) and alpha-ketoglutarate dehydrogenase activity

in mitochondrial fragments than MPP+, and lipophilicity appears to be important

for complex I inhibition by isoquinoline derivatives. However, compared with

MPP+, isoquinoline derivatives are selective but less potent inhibitors of

NADH-linked respiration in intact mitochondria, and this appears to be a

consequence of their rate-limiting ability to cross mitochondrial membranes.

Although both active and passive processes are involved in the accumulation of

isoquinoline derivatives in mitochondria, inhibition of respiration is determined

by steric rather than electrostatic properties. Compared with

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine or MPP+, isoquinoline derivatives

show selective but relatively weak toxicity to dopamine-containing cells in

culture and following systemic or intracerebral administration to experimental

animals, which appears to be a consequence of poor sequestration of isoquinoline

derivatives by mitochondria and by dopamine-containing neurones. In conclusion,

the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-like cytotoxic characteristics

of isoquinoline derivatives and the endogenous/environmental presence of these

compounds make it conceivable that high concentrations of and/or prolonged

exposure to isoquinoline derivatives might cause neurodegeneration and

Parkinson's disease in humans.

 

PMID: 9776302

 

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

[6] Isoquinolines as Neurotoxins: Action and Molecular Mechanism

 

Agnieszka Wąsik and Lucyna Antkiewicz-Michaluk

 

PDF: http://www.springer.com/cda/content/document/cda_downloaddocument/9781461415411-c1.pdf

 

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

[7] J Ethnopharmacol. 2000 Nov;73(1-2):153-9.

In vitro pharmacological activity of the tetrahydroisoquinoline salsolinol

present in products from Theobroma cacao L. like cocoa and chocolate.

 

Melzig MF(1), Putscher I, Henklein P, Haber H.

 

Author information:

(1)Institute of Pharmacy, Humboldt University, Goethestr. 54, 13086, Berlin,

Germany. matthias=melzig@pharma.hu-berlin.de

 

Cocoa and chocolate contain the tetrahydroisoquinoline alkaloid salsolinol up to

a concentration of 25 microg/g. Salsolinol is a dopaminergic active compound

which binds to the D(2) receptor family, especially to the D(3) receptor with a

K(i) of 0.48+/-0.021 micromol/l. It inhibits the formation of cyclic AMP and the

release of beta-endorphin and ACTH in a pituitary cell system. Taking the

detected concentration and the pharmacological properties into account,

salsolinol seems to be one of the main psychoactive compounds present in cocoa

and chocolate and might be included in chocolate addiction.

 

PMID: 11025151

 

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

[8] J Neural Transm Suppl. 2000;(58):111-21.

Involvement of endogenous N-methyl®salsolinol in Parkinson's disease: induction

of apoptosis and protection by (-)deprenyl.

 

Naoi M(1), Maruyama W, Takahashi T, Akao Y, Nakagawa Y.

 

Author information:

(1)Department of Brain Sciences, Institute of Applied Biochemistry, Mitake, Gifu,

Japan. mnaoi@quartz.ocn.ne.jp

 

An endogenous dopamine-derived N-methyl®salsolinol has been suggested to be

involved in the pathogenesis of Parkinson's disease. In Parkinson's disease, the

level of N-methyl®salsolinol increased in cerebrospinal fluid and the high

activity of a synthesizing enzyme, ®salsolinol N-methyltransferase, was

detected in lymphocytes. This isoquinoline induced apoptotic DNA damage in human

dopaminergic neuroblastoma SH-SY5Y cells. Among catechol isoquinolines, only

N-methylsalsolinol induced apoptosis in the cells, and the scavengers of hydroxyl

radicals and antioxidants suppressed DNA damage, suggesting that reactive oxygen

species initiate apoptosis. The isoquinoline activated caspase-3 like proteases

and a caspase-3 inhibitor protected the cells from DNA damage. (-)Deprenyl, but

neither clorgyline nor pargyline, prevented apoptotic cell death. The mechanism

of the protection was due to stabilization of mitochondrial membrane potential

reduced by the toxin. In Parkinson's disease apoptosis may be induced in dopamine

neurons by this endogenous neurotoxin, and (-)deprenyl may protect them from

apoptotic death process.

 

PMID: 11128601

 

--------

[9] Alcohol Clin Exp Res. 2010 Feb;34(2):242-50. doi:

10.1111/j.1530-0277.2009.01087.x. Epub 2009 Nov 24.

 

A critical evaluation of influence of ethanol and diet on salsolinol enantiomers

in humans and rats.

 

Lee J(1), Ramchandani VA, Hamazaki K, Engleman EA, McBride WJ, Li TK, Kim HY.

 

Free full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858379/

 

BACKGROUND: (R/S)-Salsolinol (SAL), a condensation product of dopamine (DA) with

acetaldehyde, has been speculated to have a role in the etiology of alcoholism.

Earlier studies have shown the presence of SAL in biological fluids and

postmortem brains from both alcoholics and nonalcoholics. However, the

involvement of SAL in alcoholism has been controversial over several decades,

since the reported SAL levels and their changes after ethanol exposure were not

consistent, possibly due to inadequate analytical procedures and confounding

factors such as diet and genetic predisposition. Using a newly developed mass

spectrometric method to analyze SAL stereoisomers, we evaluated the contribution

of ethanol, diet, and genetic background to SAL levels as well as its

enantiomeric distribution.

METHODS: Simultaneous measurement of SAL enantiomers and DA were achieved by high

performance liquid chromatography-tandem mass spectrometry (HPLC/MS/MS). Plasma

samples were collected from human subjects before and after banana (a food rich

in SAL) intake, and during ethanol infusion. Rat plasma and brain samples were

collected at various time points after the administration of SAL or banana by

gavage. The brain parts including nucleus accumbens (NAC) and striatum (STR) were

obtained from alcohol-non-preferring (NP) or alcohol-preferring (P) rats as well

as P-rats which had a free access to ethanol (P-EtOH).

RESULTS: Plasma SAL levels were increased significantly after banana intake in

humans. Consistently, administration of banana to rats also resulted in a drastic

increase of plasma SAL levels, whereas brain SAL levels remained unaltered. Acute

ethanol infusion did not change SAL levels or R/S ratio in plasma from healthy

humans. The levels of both SAL isomers and DA were significantly lower in the NAC

of P rats in comparison to NP rats. The SAL levels in NAC of P rats remained

unchanged after chronic free-choice ethanol drinking. There were decreasing

trends of SAL in STR and DA in both brain regions. No changes in enantiomeric

ratio were observed after acute or chronic ethanol exposure.

CONCLUSIONS: SAL from dietary sources is the major contributor to plasma SAL

levels. No significant changes of SAL plasma levels or enantiomeric distribution

after acute or chronic ethanol exposure suggest that SAL may not be a biomarker

for ethanol drinking. Significantly lower SAL and DA levels observed in NAC of P

rats may be associated with innate alcohol preference.

 

PMCID: PMC2858379

PMID: 19951298

 

----------

[10] Neurotox Res. 2015 Apr;27(3):300-13. doi: 10.1007/s12640-014-9511-y. Epub 2014

Dec 24.

 

Salsolinol, an endogenous compound triggers a two-phase opposing action in the

central nervous system.

 

Możdżeń E(1), Kajta M, Wąsik A, Lenda T, Antkiewicz-Michaluk L.

 

Author information:

(1)Department of Neurochemistry, Institute of Pharmacology Polish Academy of

Sciences, 12 Smętna Street, 31-343, Kraków, Poland, mozdzen@if-pan.krakow.pl.

 

Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline), an endogenous

compound present in the brain, was suspected of participation in the

etiopathogenesis of Parkinson's disease, the most common serious movement

disorder worldwide. In this study, we evaluated the effect of different (50, 100,

and 500 µM) concentrations of salsolinol on markers of glutamate-induced

apoptotic and neurotoxic cell damage, such as caspase-3 activity, lactate

dehydrogenase (LDH) release, and the loss of mitochondrial membrane potential.

Biochemical data were complemented with the cellular analysis, including Hoechst

33342 and calcein AM staining, to visualize apoptotic DNA-fragmentation and to

assess cell survival, respectively. The assessment of all investigated parameters

was performed in primary cultures of rat or mouse hippocampal and striatum cells.

Our study showed that salsolinol had biphasic effects, namely, at lower

concentrations (50 and 100 µM), it demonstrated a distinct neuroprotective

activity, whereas in the highest one (500 µM) caused neurotoxic effect.

Salsolinol in concentrations of 50 and 100 µM significantly antagonized the

pro-apoptotic and neurotoxic effects caused by 1 mM glutamate. Salsolinol

diminished the number of bright fragmented nuclei with condensed chromatin and

increased cell survival in Hoechst 33342 and calcein AM staining in hippocampal

cultures. Additionally, in the low 50 µM concentration, it produced a significant

inhibition of glutamate-induced loss of membrane mitochondrial potential. Only

the highest concentration of salsolinol (500 µM) enhanced the glutamate

excitotoxicity. Ex vivo studies indicated that both acute and chronic

administration of salsolinol did not affect the dopamine metabolism, its striatal

concentration or α-synuclein and tyrosine hydroxylase protein level in the rat

substantia nigra and striatum. Summarizing, the present studies exclude

possibility that salsolinol under physiological conditions could be an endogenous

factor involved in the neurogenerative processes; conversely, it can exert a

protective action on nerve cells in the brain. These findings may have important

implications for the development of the new strategies to treat or prevent neural

degeneration.

 

PMCID: PMC4353863

PMID: 25537852

 

-----------

[11] Neurology. 2005 Mar 22;64(6):1047-51.

Consumption of milk and calcium in midlife and the future risk of Parkinson

disease.

 

Park M(1), Ross GW, Petrovitch H, White LR, Masaki KH, Nelson JS, Tanner CM, Curb

JD, Blanchette PL, Abbott RD.

 

Author information:

(1)Korea University Genomic Institute, College of Medicine, Korea University,

Ansan-Si, Republic of Korea.

 

OBJECTIVE: To examine the relation between milk and calcium intake in midlife and

the risk of Parkinson disease (PD).

METHODS: Findings are based on dietary intake observed from 1965 to 1968 in 7,504

men ages 45 to 68 in the Honolulu Heart Program. Men were followed for 30 years

for incident PD.

RESULTS: In the course of follow-up, 128 developed PD (7.1/10,000 person-years).

Age-adjusted incidence of PD increased with milk intake from 6.9/10,000

person-years in men who consumed no milk to 14.9/10,000 person-years in men who

consumed >16 oz/day (p = 0.017). After further adjustment for dietary and other

factors, there was a 2.3-fold excess of PD (95% CI 1.3 to 4.1) in the highest

intake group (>16 oz/day) vs those who consumed no milk. The effect of milk

consumption on PD was also independent of the intake of calcium. Calcium from

dairy and nondairy sources had no apparent relation with the risk of PD.

CONCLUSIONS: Findings suggest that milk intake is associated with an increased

risk of Parkinson disease. Whether observed effects are mediated through

nutrients other than calcium or through neurotoxic contaminants warrants further

study.

 

PMID: 15781824

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I'm happy to report I received the Crio Bru brewing chocolate I ordered from Amazon. I brewed it two ways, using a french press per the instructions and using an Aeropress with a paper filter. I didn't perceive much difference between the two brewing techniques, and in general was quite pleased with the result.

 

In terms of richness, the resulting beverage was about 1/2 way between coffee and hot chocolate. It obviously doesn't have the mouth feel of full-fat chocolate, so anyone looking for the complete chocolate experience will be disappointed. But I consider it a worthwhile tradeoff to eliminate (or at least greatly reduce) exposure to cadmium and saturated fat, while retaining (I believe, based on the evidence) most of the beneficial cacao polyphenols.

 

From now on I plan to consume my chocolate primarily in this brewed form, using the Aeropress and a metal filter (yes Michael - I broke down and ordered one, despite the uncertainty we discussed here over how well it will eliminate the potentially harmful diterpenes in coffee).

 

--Dean

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Mike Lustgarten, a health blogger and active member of the CRS Facebook Group, pointed me to a fascinating blog post he did on the Kuna Indians of Panama and their health-promoting habit of brewing chocolate.

 

The Kuna are suprisingly healthy given their relatively primitive living conditions and poverty. In particular, they have very low rates of CVD and cancer, and don't exhibit an age-related increase in blood pressure, despite a salt intake that is at least as high as people from the US or mainland Panama, where hypertension rates are very high. Being relatively poor, they eat a pretty traditional, mostly plant-based diet with quite a bit of fish but little other meat. So that might be part of the explanation for their health.

 

But researchers think their health might also be linked to their high consumption of a banana-sweetened cacao beverage they brew from locally-harvested, raw cacao beans. From Mike's blog post about the Kuna:

 

It’s important to note that the cocoa ingested by the Kuna is naturally very rich in a specific subclass of flavonoids known as flavanols, including epicatechin, catechin, and flavanol-based oligomers known as procyanidins (Chevaux et. al 2001, Fisher and Hollenberg 2005). Kuna cocoa beans provide 3000 mg/100g flavanols. Kuna cocoa powder provides less (flavanols are lost during the fermentation process), at ~2000 mg/100g cocoa. In contrast, 6 commercially available cocoa powders /cocoa drinks didn’t exceed 150 mg flavanols/100g cocoa (Fisher and Hollenberg 2005). High levels of flavanol have been shown to reduce risk of death from coronary artery disease by as much as 58% (Mukamal et al. 2002).

 

Here is a neat video of the process the Kuna use to brew their chocolate.

 

More evidence that brewing chocolate may be the way to go...

 

--Dean

 

References from Mike's blog post

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

 

-----------

J Cardiovasc Pharmacol. 2006;47 Suppl 2:S103-9; discussion 119-21.

Hypertension, the Kuna, and the epidemiology of flavanols.

McCullough ML(1), Chevaux K, Jackson L, Preston M, Martinez G, Schmitz HH,
Coletti C, Campos H, Hollenberg NK.

A low sodium diet has often been implicated in the protection of low blood
pressure populations from hypertension, but several other dietary factors,
including those as yet unidentified, may also be involved. The Kuna Indians of
Panama are free of hypertension and cardiovascular disease, but this is changing
with migration to urban areas. We compared the indigenous diet of Kuna Indians
living on remote islands in Panama (Ailigandi), whose lifestyle is largely
hunter-gatherer, with those who have moved to a suburb of Panama City (Vera
Cruz). Between April and October 1999, members of a Kuna research team
administered a 118-item food frequency questionnaire to133 adult Kuna from
Ailigandi and 183 from Vera Cruz. Single 24-hour urine collections and nonfasting
blood samples were obtained. The Kuna in Ailigandi reported consuming a 10-fold
higher amount of cocoa-containing beverages, 4 times the amount of fish, and
twice the amount of fruit as urban Kuna
(P<0.05 by t test). Salt added was ample
among those living in Ailigandi and Vera Cruz according to both self-report
(7.1+/-1.1 and 4.6+/-0.3 tsp weekly) and urinary sodium levels (177+/-9 and
160+/-7 mEq Na/g creatinine), respectively. The low blood pressure of
island-dwelling Kuna does not seem to be related to a low salt diet. Among
dietary factors that varied among migrating Kuna, the notably higher intake of
flavanol-rich cocoa is a potential candidate for further study.


PMID: 16794446

 

Bayard V, Chamorro F, Motta J, Hollenberg NK. Does flavanol intake influence mortality from nitric oxide-dependent processes? Ischemic heart disease, stroke, diabetes mellitus, and cancer in Panama. Int J Med Sci. 2007 Jan 27;4(1):53-8.
 
Chevaux KA, Jackson L, Villar ME, et al. Proximate mineral and procyandin content of certain foods and beverages consumed by Kuna Amerinds of Panama. J Food Composit Anal. 2001;14: 553–563.
 
Fisher NDL, Hollenberg NKH. Flavanols for cardiovascular health: the science behind the sweetness. J Hypertension. 2005;23: 1453–1459.
 
Fontana L, Meyer TE, Klein S, Holloszy JO. Long-term low-calorie low-protein vegan diet and endurance exercise are associated with low cardiometabolic risk. Rejuvenation Res. 2007 Jun;10(2):225-34.
 
Hollenberg NK, Martinez G, McCullough M, et al. Aging, acculturation, salt intake, and hypertension. Hypertension. 1997; 29:171–176.
 
McCullough ML, Chevaux K, Jackson L, Preston M, Martinez G, Schmitz HH, Coletti C, Campos H, Hollenberg NK. Hypertension, the Kuna, and the epidemiology of flavanols. J Cardiovasc Pharmacol. 2006;47 Suppl 2:S103-9; discussion 119-21.
 
Mukamal KJ, Maclure M, Muller JE, Sherwood JB, Mittleman MA. Tea consumption and mortality after acute myocardial infarction. Circulation 2002; 105:2476–2481.
 
 
Warensjö E, Sundström J, Vessby B, Cederholm T, Risérus U. Markers of dietary fat quality and fatty acid desaturation as predictors of total and cardiovascular mortality: a population-based prospective study. Am J Clin Nutr. 2008 Jul;88(1):203-9.

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But researchers think their health might also be linked to their high consumption of a banana-sweetened cacao beverage they brew from locally-harvested, raw cacao beans. From Mike's blog post about the Kuna:

 

It’s important to note that the cocoa ingested by the Kuna is naturally very rich in a specific subclass of flavonoids known as flavanols, including epicatechin, catechin, and flavanol-based oligomers known as procyanidins (Chevaux et. al 2001, Fisher and Hollenberg 2005). Kuna cocoa beans provide 3000 mg/100g flavanols. Kuna cocoa powder provides less (flavanols are lost during the fermentation process), at ~2000 mg/100g cocoa. In contrast, 6 commercially available cocoa powders /cocoa drinks didn’t exceed 150 mg flavanols/100g cocoa (Fisher and Hollenberg 2005). High levels of flavanol have been shown to reduce risk of death from coronary artery disease by as much as 58% (Mukamal et al. 2002).

 

Interesting post Dean.

 

This brought to mind the flavOnol/flavAnol mess.

 

I had to refresh my understanding, so for what it's worth here it is:

 

https://en.wikipedia.org/wiki/Flavonoid

Flavonoids (or bioflavonoids) are a class of plant secondary metabolites.

Flavonoids are widely distributed in plants, fulfilling many functions. Flavonoids are the most important plant pigments for flower coloration, producing yellow or red/blue pigmentation in petals designed to attract pollinator animals.

Chemically, they have the general structure of a 15-carbon skeleton, which consists of two phenyl rings (A and B) and C is a heterocyclic ring.

  • Flavanoids such as the catechins are "the most common group of polyphenolic compounds in the human diet and are found ubiquitously in plants".
  • Flavonols, the original bioflavonoids such as quercetin, are also found ubiquitously, but in lesser quantities.
Flavonoid Subgroups

3.1 Anthoxanthins

3.2 Flavanones

3.3 Flavanonols

3.4 Flavans

3.5 Anthocyanidins

 

So flavOnols are in group Anthoxanthins, while flavAnols are in group Flavans.

  • Flavans include:
    • flavan-3-ols (flavanols): Catechin, Gallocatechin (GC), Catechin 3-gallate (Cg),

      Gallocatechin 3-gallate (GCg)), Epicatechins (Epicatechin (EC)),

      Epigallocatechin (EGC), Epicatechin 3-gallate (ECg),

      Epigallocatechin 3-gallate (EGCg)

      Proanthocyanidins are dimers, trimers, oligomers, or polymers of the flavanols

    • flavan-4-ols
    • flavan-3,4-diols
  • Anthoxanthins are divided into two groups:
    • Flavone: e.g. Luteolin, Apigenin, Tangeritin
    • Flavonol: e.g. Quercetin, Kaempferol, Myricetin, Fisetin, Galangin,

      Isorhamnetin, Pachypodol, Rhamnazin, Pyranoflavonols,

      Furanoflavonols,

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On metals/unwanteds (cd, al, pb, etc.) in in cacao I gave up eating whole, skin-on cacao beans because of the contaminants risks and also due to all the saturated fat (I was eating over 2 oz/day). I now get my cacao only from wildernessfamilynaturals who has provided very good tested numbers, and I consume their defatted powder (less than an oz/day due to the higher caffeine/oz concentration).  on green tea, i still eat it but don't do white tea anymore (due to it’s China origin); and I buy only from sugimotousa (which offers very lightly steamed sencha) and has has provided very good test results on all the metals/toxins that concern me.

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Thanks Kenton, and nice to hear from you!

 

While I brew and filter almost all of my cacao these days (from raw beans I grind myself, and mix with ground coffee & tea - per earlier in this thread), I do still consume a small amount of cacao powder per day. So you information is very helpful.

 

For anyone interested, here is the link to Wilderness Family Naturals (WFN) web store page for their raw, non-fermented cacao powder, which includes heavy metal test results. Here are the results, which are quite recent, and they should be commended for testing and for posting the test results:

 

Raw Cacao Laboratory Testing Results

*ppm = parts per million

 

Non-Fermented Raw Cacao Powder (2 different suppliers)

8/6/2015
Arsenic   0.049 ppm
Cadmium   0.704 ppm
Lead   0.288 ppm
Mercury   <0.02 ppm


6/9/2015
Arsenic   0.037 ppm
Cadmium   0.674 ppm
Lead   0.154 ppm
Mercury   <0.01 ppm

 

So Cadmium in WFN raw cacao powder is about 0.7 ppm, which is equivalent to 0.7 mcg/g (micrograms cadmium per gram of cacao powder). The US regulatory "Maximum Allowable Daily Level" (MADL) for oral cadmium is 4.1 mcg/day. That works out to about 6g of WFN cacao powder - almost exactly a teaspoon. Your "less than an oz/day" of WFN cacao powder (~25g?) equates to something like 6 times the MADL for cadmium. Isn't that a bit high? Or am I missing something?

 

Based on this information, I may (sadly) cut out the small amount of raw cacao powder I've been eating entirely, in favor of consuming chocolate via my brewing & filtering method, which I continue to employ and enjoy.

 

--Dean

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Thanks Kenton, and nice to hear from you!

 

While I brew and filter almost all of my cacao these days (from raw beans I grind myself, and mix with ground coffee & tea - per earlier in this thread), I do still consume a small amount of cacao powder per day. So you information is very helpful.

 

For anyone interested, here is the link to Wilderness Family Naturals (WFN) web store page for their raw, non-fermented cacao powder, which includes heavy metal test results. Here are the results, which are quite recent, and they should be commended for testing and for posting the test results:

 

Raw Cacao Laboratory Testing Results

*ppm = parts per million

 

Non-Fermented Raw Cacao Powder (2 different suppliers)

8/6/2015

Arsenic   0.049 ppm

Cadmium   0.704 ppm

Lead   0.288 ppm

Mercury   <0.02 ppm

6/9/2015

Arsenic   0.037 ppm

Cadmium   0.674 ppm

Lead   0.154 ppm

Mercury   <0.01 ppm

 

So Cadmium in WFN raw cacao powder is about 0.7 ppm, which is equivalent to 0.7 mcg/g (micrograms cadmium per gram of cacao powder). The US regulatory "Maximum Allowable Daily Level" (MADL) for oral cadmium is 4.1 mcg/day. That works out to about 6g of WFN cacao powder - almost exactly a teaspoon. Your "less than an oz/day" of WFN cacao powder (~25g?) equates to something like 6 times the MADL for cadmium. Isn't that a bit high? Or am I missing something?

 

Based on this information, I may (sadly) cut out the small amount of raw cacao powder I've been eating entirely, in favor of consuming chocolate via my brewing & filtering method, which I continue to employ and enjoy.

 

--Dean

I spoke with the guys at "Health Ranger" and asked about their raw cacao nibs.  Their most recent lot was certified at < 0.5ppm cadmium.  Not much better, but a slightly better score.  6g is usually around all I need in a day for adding some chocolate as a sort of spice.

 

How much do you usually add to your brewed beverage?

 

This is an interesting way to consume cocoavia's powder, which is marketed as containing "the highest concentration of cocoa flavanols per serving in a dietary supplement" as a matcha-style tea:

WXW3Tve.png

 

Although I'm not a fan of the maltodextrin they use to sweeten their "unsweetened" cacao.

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Sirtuin wrote:

 

How much [ground cacao beans] do you usually add to your brewed beverage?

 

I'm brewing 60g / day of a 50/50 mix of ground coffee and cacao beans, plus another 10-12g of mixed teas. So about 30g/day of ground cacao. I mix it all up with about 40oz of water.

 

I cold brew overnight on the counter, and then do a brief hot brew (2 min) of the solids with a fresh 12oz of water to extract the remaining polyphenols and caffeine that weren't extracted in the cold brew. Then I strain out the solids, and then pass the 60+oz of liquid through 4 paper coffee filters to sift out the heavy metal & saturated fat-containing sediment.

 

What remains is a dark but clear (not cloudy) liquid, like filtered coffee or tea. It is quite tasty.

 

--Dean

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Dean - First, those two sets of data from the wildernessfamilynaturals (WFN) are in error; they cut out the supplier with the higher numbers of the two sets of numbers you reproduced.  Second, the lowest tested cacao is their non-fermented cacao nibs--check it out.  BTW, I have an aeropress and every day the past week I have been grinding/brewing/filtering my left over inventory of whole beans.  I do 60g/day (sometimes 30g/day only) of whole raw skin on nonfermented org cacao beans.  I grind them up in the morning, dump 100C water on them, then filter/drink around 2pm--it's satisfying to me to not eat the cacao dry roasted like the chofee providers (like the one you and I buy from) do!  Back on the WFN topic, I really like non-fermented aspect which is special for the WFN I think.  BTW2, thanks for the vote of confidence in interpreting my "less than an oz/day" to mean ~25g, ha!  The number I had consumed the one day I consumed the powder was 10g.

Edited by Kenton

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Kenton,

 

Dean - First, those two sets of data from the wildernessfamilynaturals (WFN) are in error; they cut out the supplier with the higher numbers of the two sets of numbers you reproduced.

 

OK - but they weren't that different (0.67 vs. 0.70 mcg/g). 

 

 Second, the lowest tested cacao is their non-fermented cacao nibs--check it out.

 

Yes - the nibs have about 1/2 the cadmium per gram of the powder, but the nibs also contain twice the calories and 3x the saturated fat of cacao powder. Plus, you said you "consume their defatted powder", which I assumed was their cacao powder. Do you consume their nibs as well?

 

... it's satisfying to me to not eat the cacao dry roasted like the chofee providers (like the one you and I buy from) do!

 

I bought a pound of ground brewing cacao from one of the brewing chocolate providers (Crio Bru), as a test to see what it was like. I've used it up and am now grinding my own raw cacao beans for brewing purposes. I didn't see any taste advantage to the Crio Bru, it was more expensive than whole beans, and like you, I'm not thrilled with the roasting - if nothing else the roasting reduces the polyphenol content.

 

thanks for the vote of confidence in interpreting my "less than an oz/day" to mean ~25g, ha! 

 

It wasn't a vote of (dis)confidence - I was interpreting your statement "less than an oz/day" as I would use it - i.e. less than an ounce, but pretty close to an ounce. 

 

The number I had consumed the one day I consumed the powder was 10g.

 

If I was referencing something that was a lot less than an oz, like 10g, I'd either say "10g", or (less likely) "about 1/3 oz". But that's just me.

 

I'm confused, by the statement "the one day I consumed the powder" are you saying you don't eat the WFN cacao powder? I thought from your original post (" I consume their defatted powder") that was what you do eat!?

 

--Dean

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I appreciate the expressed sensitivity to the Cd numbers.  Per (11) below however the differences in Cd may be somewhat academic.  Further, let us hope the grind/ steep/ mild brew/ filter/ drink (as a clear beverage) process, while removing Cd, does not also remove the reasons why we seek to consume cacao.  Is there evidence of consumption of a clear cacao extract as your post describes benefiting experimental subjects?  On the topic of WFN, I've bought samples of WFN's powder and their "pristine" nibs.  Hence, I have done the WFN powder once mostly because I'm cleaning out my pounds of inventory of whole cacao beans.  The powder was/is a contemplated/tested best replacement for my 60g whole cacao beans per day much-loved routine of many years.  So, on the powder vs. the nibs balance as to which to move to in the future, based on a balance of criteria (1) saturated fat, (2) nasties, (3) time to CONSUME (i liked to nibble on my 60g whole beans during a 2-3 HOUR feeding window and was very satisfied (see item 6) and not tempted to eat more or to eat anything else (hence, I was able to restrict total calorie intake for the day without deprivation on the 60g beans/day))--the powder is similar in this regard yet the nibs are not as i can inhale the nibs in minutes like cashew or mac nuts, ha, (4) ability to eat raw without heat (e.g., boiling-water) processing, (5) confidence in consuming important parts of the cacao instead of throwing out nutritive parts as grinds, (6) satiability--the powder satisfies me in ways referenced above and in using cacao eating to extend a daily low-blood-sugar fasting period, (7) likelihood that I will not overeat (ref'd above) AND will not feel like I am "dieting" by restricting amount of consumption--I try to eat mostly/entirely ad lib & never feel deprived or limit what I wish to put in my pie hole, (8) dramatically less time to PREPARE the powder (i eat it dry/stright-up) as compared to the time to process raw nibs or beans for drinking as you may appreciate <wink>, (9) again, ref’g my concern with throwing out the "grinds" as: including beneficial nutrition I may wish to consume and as (10) wasteful of food (save the planet) in general, the powder appears suitable for me.  Additionally, as an item (11), the Cd in our diets I am told by Navitas is relevant, too, to the Cd we are trying to control/minimize in cacao consumption for the total Cd intake equation.  Navitas says “[m]any foods have trace levels of cadmium, including meats, grains, vegetables (especially leafy greens), nuts, and seeds” and provides an example showing the ppm Cd in spinach and sunflower seeds appears to be about the same as in cacao powder.  'Not condoning anything yet wondering if other tactics or dietary alterations may be indicated as equally or more relevant as compared to this phenylethlamine amped "happy cacao" tripping.

Edited by Kenton

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Kenton,

 

 Is there evidence of consumption of a clear cacao extract as your post describes benefiting experimental subjects?

 

I discussed earlier in this thread why I'm pretty certain that brewing cacao will extract the healthy polyphenols based on the fact that this method works very well to extract the polyphenols from two other plant-based brewed beverages - coffee and tea. Coffee beans in particular are quite similar to cacao beans, and from all the evidence for brewed, filtered ground coffee beans, the polyphenols do get extracted to the liquid, rather than sticking with the grounds, and do make it through paper filters into the cup.

 

(5)  confidence in consuming important parts of the cacao instead of throwing out nutritive parts as grinds

 

Is there evidence that the good stuff stays with the grounds when one brews cacao? It would seem that by this logic, you'd also want to consider consuming spent coffee grounds, since who knows what healthy nutrients remain in the grounds after the coffee brewing process.

 

It seems plausible to me to postulate that the reason we brew coffee beans rather than eat them (except when chocolate covered! :Dxyz ) and eat cacao beans (usually after heavy processing and adding sugar to remove bitterness and improve palatability) rather than brew them, is little more than a historical accident. 

 

(11) the Cd in our diets I am told by Navitas is relevant too to the Cd we trying to control/minimize via cacao consumption.  Navitas says “[m]any foods have trace levels of cadmium, including meats, grains, vegetables (especially leafy greens), nuts, and seeds” and provides an example showing the ppm Cd in spinach and sunflower seeds is about the same as in cacao powder.

 

Now this is an objection with some meat on it  :)xyz . I did some research, focusing on leafy greens, since that is one food Navitas emphasized and obviously most of us here at a lot of them. What I found was quite interesting, and either troubling (for vegetables) or comforting (for cacao), depending on your perspective.

 

In this new study [1] in the latest issue of Ecotoxicology and Environmental Safety, researchers in Italy investigated several different leafy greens grown on two different plots of land known not to be particularly contaminated with heavy metals and measured their cadmium content, as well as that of the soil in which they were grown.

 

First off, something interesting from the introduction in the full text:

 

Hence, Cd [Cadmium] is one of the metals for which the Food and Agricultural Organization and the World Health Organization
have set limits (FAO-WHO, 1978), with a maximum permitted human intake of 70 mcg/d.

 

The WHO's maximum of 70mcg/day is 17x higher than the the California Office of Environmental Health Hazard Assessment (OEHHA) which has a Maximum Allowable Daily Level (MADL) for oral cadmium of 4.1 mcg/day. It seems like the California regulators may have built in quite a bit more of a safety margin than the WHO when setting the acceptable limit on Cadmium. The conservative nature of the California standard is supported by this definition in the above-referenced link:

 

The MADL is derived by dividing the NOEL [No Observable Effects Level] by one thousand (1,000) to arrive at the maximum allowable dose level.

 

In detail, the study [2] on which the California standard is based was a study of feeding Cadmium to pregnant rats in their drinking water during their pregnancy and then measuring the body weight and behavior of the pups to see if they were impacted by the cadmium. The researchers found that rats fed cadmium at the human equivalent of 4.1 mg/day (note: mg not mcg), there was no observable effect on the birthweight of the rat pups (but at twice that dose there was a detrimental effect). The OEHHA therefore divided this NOEL of 4.1 mg/d by 1000 to reach their MADL of 4.1 mcg/day.

 

So it would seem several pieces of evidence suggest the California standard for cadmium is quite conservative, perhaps bordering on overkill. But at the same time, it is interesting (and a bit troubling, IMO) that an important food safety standard like this is based on the results of a single study, of a single paradigm for measuring harm from cadmium exposure (infant rodent birthweight and behavioral development). Perhaps that is part of the reason why they build in a 1000x safety factor!

 

I wanted to check just how conservative this 4.1 mcg/day California limit was. I was fortunate to find this handy summary of several oral cadmium dosage limits from around the world. Here is what it says:

 

US EPA: Standards for drinking water are 5 mcg/L. Reference dose (maximum acceptable oral dose): 1 mcg/kg/day [~50 mcg/day for average human - 12.5x the California standard].

 

US ATSDR: [Agency for Toxic Substances and Disease Registry] Chronic durational oral minimum risk level of 0.1 mcg/kg/day (=0.7 mcg/kg/week) based on renal effects. [~5 mcg/day for average human - similar to California standard]

 

EFSA (European Food Safety Authority), 2009: Tolerable weekly intake of cadmium is 2.5 mcg/kg body weight. [~18 mcg/day for average human - 4.5x the California standard]

 

JECFA (Joint FAO/WHO Expert Committee on Food Additives): PTWI of 7 mcg/kg bw/week.  [~50 mcg/day for average human - 12.5x the California standard].

 

So it does indeed look like the California limit is quite conservative relative to most other regulatory agencies when it comes to oral cadmium, and the limit varies a lot (by a factor of up to ~5-17x) between them.

 

So now back to the main point - cadmium in leafy greens.

 

The researchers indeed did find (as Navitas said) reasonably elevated levels of cadmium in the two greens they tested (lettuce and endive). The cadmium content varied depending on several factors, including the farm site, fertilizer type, leafy green type, and whether the sampled leaves were young or mature. The range of cadmium across all these variations was 0.6 - 3.8 mcg/g dry weight. Since leafy greens are about 90% water, this isn't quite as bad as it seems, but it is still pretty bad.

 

For comparison, recall that the Wilderness Family Naturals cacao powder reported a cadmium level of about 0.7 mcg/g, which is obviously a dry weight (cacao powder is about as dry as it gets). 

 

So in short, dehydrated leafy greens appear to have comparable or higher levels of cadmium than cacao powder, which was the most concentrated source of cadmium among the chocolate products.

 

Ignoring the dehydrated part, since it seems likely that many of us eat fresh leafy greens in quantities easily 10x that of cacao powder that effectively offsets the dry/fresh weight distinction, study [1] suggests we should perhaps be equally concerned (or unconcerned?) about cadmium overload from vegetable sources as we are about cacao.  

 

On balance, since leafy greens have been shown in study after study to be about the healthiest food you can eat, perhaps the cadmium concern in chocolate products may be overblown.

 

--Dean

 

---------

[1] Ecotoxicol Environ Saf. 2016 Jan;123:89-94. doi: 10.1016/j.ecoenv.2015.05.019.

Epub 2015 May 23.

Cadmium accumulation in leaves of leafy vegetables.

Baldantoni D(1), Morra L(2), Zaccardelli M(3), Alfani A(4).

 

Full text vis Sci-Hub.io: http://www.sciencedirect.com.sci-hub.io/science/article/pii/S0147651315002420

Leafy vegetables have a relatively high potential for Cd uptake and
translocation, and are thus considered Cd accumulators. For this reason, leaves
and roots of lettuce (Lactuca sativa L.) and endive (Cichorium endivia L.)
plants, grown on different agricultural soils in Campania region (southern
Italy), subjected to different fertilisation treatments (unfertilisation, compost
amendment and mineral fertilisation), were analysed for Cd concentrations.
Moreover, to clarify if the highest concentrations found are linked to older and
inedible or to younger and edible leaves, external and internal endive leaves
were separately analysed. All the leafy vegetables analysed showed on average
2-fold higher Cd concentrations in leaves than in roots. Leaf Cd concentrations
in both lettuce and endive plants significantly differed among fertilisation
treatments, with values highest in the plants grown on mineral fertilised soils.
Apart from the soil fertilisation treatments, however, Cd leaf concentrations
were often higher (up to 4-fold) than the threshold deduced by the EU 420/2011
Regulation, although the plants grew on unpolluted soils. Anyway, external leaves
of endive plants showed significantly higher concentrations than internal leaves
(in some cases the values were 3-fold higher), partly reassuring on the
consumption of the younger leaves. Moreover, this study points out two major
drawbacks in the Italian and European regulatory frameworks: (1) metal
concentration (as total and/or available fraction) limits in agricultural soils
are lacking; (2) metal concentration thresholds (currently existing only for Cd
and Pb in crops) reported in the EU 420/2011 Regulation, expressed on the fresh
weight basis rather than on the dry weight basis, appear not suitable.

Copyright © 2015 Elsevier Inc. All rights reserved.

PMID: 26004982

 

--------

[2] Neurobehav Toxicol Teratol. 1986 Sep-Oct;8(5):463-8.

Developmental and longterm neurobehavioral toxicity of low level in-utero cadmium
exposure in rats.

Ali MM, Murthy RC, Chandra SV.

The developmental and behavioral toxicity of gestational exposure to low levels
of cadmium (Cd, 4.2 and 8.4 micrograms/ml in drinking water) were assessed in
rats. Significant decreases in birth weight and growth rate were observed in the
8.4 micrograms Cd/ml group. The metal exposure had no effect on the ontogeny of
physical landmarks, surface and air righting reflexes and visual placing, but a
significant hyperactivity and delay in the development of cliff aversion and
swimming behavior were observed in the neonatal pups of either treatment group.
Marked decreases in the locomotor activity shuttle box performance were evident
at 60 days but not at 90 days of postnatal life. The apomorphine-induced
hyperactivity was not affected in these rats at either age. These data indicate
that Cd exposure during the critical periods of development might result in
developmental and behavioral deficits with longterm implications on adult
behavior.

PMID: 3785508

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"my BIG" was edited out of the post (to which you reply) HOURS prior to your reply, so kindly edit it out of your reply for the same reason :~)

Now, coffee is not cacao, and assuming they are the same and can be consumed the same way for benifits linked to them being consumed in different ways is a theory only --a good theory but a theory/hypothesis only.  Coffee is not consumed in a clear beverage form...and, yes, it seems to me the dark parts AND the clear parts (rather than just the extracted clear parts) of cacao are the ONLY data points we have; therefore, one might interpret the dark AND clear parts together as the ONLY evidence we have in the collective writings and actions of man on the benefits of cacoa.  My logic, however, tells me that the clear extraction is fine and dandy for a good healthy life. summing up, i'm a layperson not researched on the topic so am posing the above as interpretations of the topic.

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Kenton,

 

"my BIG" was edited out of the post (to which you reply) HOURS prior to your reply, so kindly edit it out of your reply for the same reason :~)

 

Fair enough - but it takes me hours to compose a thoroughly-researched response like the one you reference, so I can hardly be blamed for quoting an earlier version of your post.

 

Per your request, I've edited my post to reflect your revised (less emphatic) wording regarding your reservations about throwing out cacao grounds due to concerns over missing out on nutrition in them.

 

Coffee is not consumed in a clear beverage form...

 

You've lost me on this one. Some coffee (like french press or espresso) is indeed pretty cloudy. But the benefits of coffee have largely been demonstrated via paper-filtered coffee, which is how the vast majority of people in the US consume it, and which in my judgement has a level of clarity / translucency pretty much equivalent to brewed cacao as I've prepared it.

 

Furthermore, when coffee has been shown to have detrimental effects, it has been for unfiltered coffee which allows components like the the LDL-cholesterol-raising diterpenes (see this post/thread) to remain in the 'fines' (cloudy stuff and sediment at the bottom) of coffee.

 

My logic, however, tells me that the clear extraction is fine and dandy for a good healthy life.

 

We're on the same page on this one!

 

--Dean

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-Historical Coffee Bean - roast,                     grind, hot brew, filter.

-Historical Tea               - roast/steam,        (grind), hot brew, (filter).

-Clear Cacao Drink       - FERMENT, RAW, grind, brief hot brew, filter

The three techniques may be less than closely aligned/analogous.  I agree with you that "the benis" are likely adequately extracted, yet would agree more if this were tested by a Lab.  (Years ago I favored dried raw Black Botija Olives (BBOs) over olive oil (OO), so much that I had a serving tested and compared to the OO; the resuts favored the BBOs over the OO for the sought nutrition.

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