Like many of you, I see patients in the longer term for a variety of reasons.
Health and wellness through to pain relief for intractable issues.
One such patient I have seen for nearly a decade, has AS, not active anymore but it sure left him stiff.
As a result I have seen him every 6 weeks for many years, and more recently in 2023 he started to get a few issues with his heart.
First a bout of tachycardia, then suddenly a diagnosis of significant heart disease with two stents fitted and a defibrillator, plus statins, clopidogrel and rivaroxaban.
He also had atrial fibrillation ongoing.

As you can see, I advised him with reference to CoQ10 and the statins use, plus vitamin D and also for statins.
I sent him the article from this newsletter so he understood why this is so important.
Remember, statins block cholesterol production, but this lowers Co ENZYME Q-10 a rate limiter for energy production.

So, they get tired and the tissues with the highest energy demand complain, often muscles, hence terrible muscle pain.

But, remember his heart is not healthy, and the heart is a muscle, and it has to contract every second or so.
Think about that, many people get muscle pain from low energy via CoQ10 depletion, and your heart is diseased, working the hardest of all the muscles, that is tricky.

Does it work? Yes.

Re-fresh your memory 👇

I ensured his vitamin D was good, as statins stop that too, as it is made from cholesterol.
Click to re-remember 👇

Plus the great irony, statins interfere with your vitamin K cycle, and vitamin K determines where your calcium ends up. Ideally, in your bone under the control of K, but if not, then into your…….arteries (I am not making this up).

Note CACS stands for Coronary Calcification Arterial Score, dark blocks are no statins, grey blocks are statin users.

Whether you have known CVD or are looking for prevention, it still increases calcification in your arteries.
NOTE: This is slightly hard to believe isn’t it?
Statins actually increase the risk of arterial calcification.
But no one is arguing with that, as the science is so clear.
What they suggest is, yes, statins do increase arterial calcification BUT they make the plaques more stable.

They conclude
“….meta-analyses of the available trials have shown a significant reduction of risk of cardiovascular events (Here they mean relative risk reduction, which means very low single digit % risk reduction in real terms). In contrast, statins accelerated CAC. This suggests that statin-mediated atheroma calcification may enhance plaque stability and reduce the risk of plaque rupture”
Note, they have no real evidence for this idea. It increases calcification BUT reduces heart attacks (relatively), and so they are theorising about how it happens.
But of course, the % reduction is thinner than my hairline and often missing in studies not funded by independent researchers.
Plus the mechanism for any benefits is likely because statins are a mild anti-inflammatory.
Below we discuss the JUPITER study where they studied people with normal cholesterol but CRP (marker of inflammation) over 2 mg/L.

Note that the NHS is not interested in your CRP unless it goes over 7.5 mg/L ish.

Thus, people with normal cholesterol got a mild anti-inflammatory and yes, there were some (albeit small) benefits.
Well, if you want to reduce your inflammation levels, might I suggest changing your diet and lifestyle rather than chugging statins?
Crazy idea, I know.
The mechanism for statins increasing calcification is the blocking of a vitamin K2-dependent protein called osteocalcin which, when carboxylated, binds calcium.
Thus, if you leave it UN-carboxylated, your calcium disappears into your soft tissues.
Thus un-carboxylated osteocalcin, a functional marker of low K2 status.
Now here is some nuance, there are different forms of K2.
The main one used by supplement companies is MK7, but the one that every single mammal puts into its breast milk and the only one to cross the placenta is MK4.

And it is the conversion of K1 into MK4 that statins block.

That conversion needs an enzyme, and they need a co-factor, usually a mineral, in this case MAGNESIUM.

How common is low magnesium? In general population:

But in clinically symptomatic people, especially those with heart issues, it is way higher.
And that, my friends, is why we use mainly MK4 in our best-selling Vitamin D/K2 sublingual.


If you are using a different brand of vitamin D/K2, check your label, I guarantee you they are using MK7 only and short changing you.
Back to my patient, note I recommended him to look at potassium levels and suggested a red blood cell POTASSIUM test.
Potassium is the most abundant INTRAcellular mineral and 98% of it is in the CELLS (ie 2% only in the blood/serum).

Thus, serum (blood) potassium tests are often NOT reflective of CELLULAR levels and thus function levels (in my patients case the heart).

We know potassium is critical in stabilising the cell membrane, so if it low we can get unstable nerves.
In the context of the heart, this is palpitations and arrhythmias, plus a lot of other very vague nebulous symptoms, especially if they occur in the elderly.

Here we see some research testing serum potassium and RBC potassium to see if they correlate and change with supplementation.

Note the highlighted yellow area under RBCK is red blood cell potassium, and this is abnormal at 88 mmol/L. The same patients also had a serum potassium that was plum optimum.
The NHS would not be interested until they went under 3.5.
So that means they are being missed.

Then, they supplemented the same patients with potassium and the RBC potassium came up to normal (remember RBC are CELLS and thus reflective of cellular levels in example, heart tissue).
The RBC potassium pops up to 97.9 mmol/L from 88.1 mmol/L, but the serum level (already optimum) does not change at all.

Now, I had acces to my patients’ blood tests and they are interesting as they inlcude potassium.

They are a little small, so see below again

If you can’t really see it, they are all with two exceptions, over 4 and at what we would call optimum, certainly none below 3.5 the level we would call deficiency.
But given what I know about potassium serum/blood tests and the fact he was suffering with atrial fibrillations that are resistant to cardioversions, I suggested he trial some potassium citrate at 1000 mg daily.
Note the RDA/RI is 2000 mg, the highest of all the minerals and very hard to achieve without supplementation.
Within 3 days, his atrial fibrillation has stopped.
His nerve and heart cells we low in potassium but his serum/blood (the transport to the cells) was normal.
That is the power of understanding some basic bits of information that I have distilled down into the Core Concepts in Chiropractic Nutrition.
I have literally done the hard work for you.
All you have to do is login and download that knowledge in 5-10 minute chunks into your brain.
It is clinical map to get you and your patients better than you ever thought.
