Recently researcher from the University of Cambridge reported that an imbalance in calcium and the Parkinson’s-associated protein alpha synuclein can cause the clustering of synaptic vesicles.
What does this mean? And should we reduce our calcium intake as a result?
In today’s post, we will review the research report, consider the biology behind the findings and how it could relate to Parkinson’s, and discuss what can or should be done.
Me and Brie. Source: Wikipedia
When I turned 25, I realised that my body no longer accepted cheese.
This was a very serious problem.
You see, I still really liked cheese.
A bottle of red wine, a baguette and a chunk of brie – is there any better combination in life?
So obviously my body and I had a falling out. And yes, it got ugly. I wanted things to keep going the way they had always been, so I tried to make things interesting with new and exotic kinds of cheeses, which my body didn’t want to know about it. It rejected all of my efforts. And after a while, I gradually started resenting my body for not letting me be who I was.
We sought help. We tried interventions. But sadly, nothing worked.
And then things got really bad: My body decided that it didn’t have room in its life for yogurt, milk or even ice cream anymore (not even ice cream!!!). Basically no dairy what so ever.
There’s something’s missing in my life. Source: Morellisices
OMG. How did you survive without ice cream?
Well, I’ll tell ye – it’s been rough.
All silliness aside though, here is what I know: It is actually very common to develop a lactase deficiency as we get older – lactase being the enzyme responsible for the digestion of whole milk. In fact, about 65% of the global population has a reduced ability to digest lactose after infancy (Source: NIH). I am not lactose intolerant (one of the few tests that I actually aced in my life), but I do have trouble digesting a particular component of dairy products – which can result in discomfort and socially embarrassing situations (one day over a drink I’ll tell you the ‘cheese fondue story’). Curiously, that mystery ingredient is also present in products that have no dairy (such as mayonnaise – it absolutely kills me).
But spare me your tears, if one is forced to drop a particular food group, dairy is not too bad (if I am ever forced to give up wine, I swear I’ll go postal).
My biggest concern when I dropped dairy, however, was “where was I going to get my daily requirements of calcium?“.
Understand that calcium is really rather important.
Why is calcium important?
The title of today’s post comes from a Rudyard Kipling poem, and it seemed appropriate as we review the results of a clinical study for Parkinson’s disease…involving bees! Much has been written about the medicinal properties of the lovely honey that bees make. The healing properties of the sweet produce of our little friends seems to cure all ailments.
Today’s post, however, is not about honey.
No, today’s post is about the other thing bees are known for: their sting!
Earlier today a group of researchers in Paris (France), published the results of a clinical trial in which they gave bee venom to people with Parkinson’s disease for 11 months.
Title: Bee Venom for the Treatment of Parkinson Disease – A Randomized Controlled Clinical Trial.
Authors: Hartmann A, Müllner J, Meier N, Hesekamp H, van Meerbeeck P, Habert MO, Kas A, Tanguy ML, Mazmanian M, Oya H, Abuaf N, Gaouar H, Salhi S, Charbonnier-Beaupel F, Fievet MH, Galanaud D, Arguillere S, Roze E, Degos B, Grabli D, Lacomblez L, Hubsch C, Vidailhet M, Bonnet AM, Corvol JC, Schüpbach M.
Journal: PLoS One. 2016 Jul 12;11(7):e0158235.
PMID: 27403743 (This study is OPEN ACCESS if you would like to read it)
No! What? Bee Venom? Really?
Yeah, I know. Weird, right? But there is actually some logic to the idea.
Bee venom has recently become in vogue for all kinds of health associated products (eg. face masks, etc – click here for more on this), but preclinical experiments have also demonstrated that it can have beneficial effects in models of Parkinson’s disease.
Bee venom (or Apitoxin as it known to the science types) contains some interesting components, one of which is called Apamin.
Apamin. Source: Wikipedia
Apamin is the only component of bees venom that can pass through the blood-brain-barrier and enter into the brain. Once inside the brain, Apamin selectively blocks structures on the membrane of cells called ‘calcium channels’.
Calcium channels allow calcium (surprise) to enter a cell, and control many physiological functions including neurotransmitter release, muscle contraction and cell survival. It has already been demonstrated in models of Parkinson’s disease that Apamin has neuroprotective properties on the dopamine neurons in the brain:
Title: Bee venom and its component apamin as neuroprotective agents in a Parkinson disease mouse model.
Authors: Alvarez-Fischer D, Noelker C, Vulinović F, Grünewald A, Chevarin C, Klein C, Oertel WH, Hirsch EC, Michel PP, Hartmann A.
Journal: PLoS One. 2013 Apr 18;8(4):e61700.
PMID: 23637888 (this article is OPEN ACCESS if you would like to read it)
The researchers in this preclinical study demonstrated that bee venom was protective in models of Parkinson’s disease. When they tested Apamin alone, however, they found that it reproduced the protective effects only partially. They concluded that other components of bee venom must be enhancing the protective action of Apamin.
So what happened in the clinical trial?
The researchers in France conducted a randomized double-blind study (meaning that nobody – researchers included – knew who was getting the bee venom or the saline control solution). They took 40 people with early stage Parkinson disease (Hoehn & Yahr stages 1.5 to 3) and assigned them to either monthly bee venom injections or equivalent injections of saline.
After 11 months of monthly injections, the researchers found that bee venom did not significantly decrease the motor features of Parkinson’s disease (as judged by UPDRS III scores during ‘off’ condition). In addition, brain imaging (DAT-scan) did not differ significantly between treatment groups over the 11 months.
The researchers did, however, see improvements in some of the cognitive measures in subjects receiving the bee venom (albeit non-significant).
In their concluding remarks, the researchers questioned whether lack of significant effect was due to the low frequency of injections (once per month). Maybe the subjects in the trial were simply receiving too little of the treatment for it to have an effect. With the support of more preclinical experimental results, they propose that a larger study is warranted with a higher administration frequency and possibly higher individual doses of bee venom.
Will this happen?
It is unclear at present.
In the study, 4 subjects had immune system responses to the bee venom, so it may be wise to firstly establish what components of bee venom are having any beneficial effect before proceeding with further clinical trials.
The banner for today’s post was sourced from modern.scot