Strange Things Happening In The Islets Of Langerhans

It is generally known and widely accepted that carbs have the biggest effect on blood sugar levels (and thus insulin response), fats less so, and protein least of all.

And yet, there was a groundbreaking study published yesterday which found:

❝Glucose is the well-known driver of insulin, but we were surprised to see such high variability, with some individuals showing a strong response to proteins, and others to fats, which had never been characterized before.

Insulin plays a major role in human health, in everything from diabetes, where it is too low*, to obesity, weight gain and even some forms of cancer, where it is too high.

These findings lay the groundwork for personalized nutrition that could transform how we treat and manage a range of conditions.❞

~ Dr. James Johnson

*saying ”too low” here is potentially misleading without clarification; yes, Type 1 Diabetics will have too little [endogenous] insulin (because the pancreas is at war with itself and thus isn’t producing useful quantities of insulin, if any). Type 2, however, is more a case of acquired insulin insensitivity, because of having too much at once too often, thus the body stops listening to it, “boy who cried wolf”-style, and the pancreas also starts to get fatigued from producing so much insulin that’s often getting ignored, and does eventually produce less and less while needing more and more insulin to get the same response, so it can be legitimately said “there’s not enough”, but that’s more of a subjective outcome than an objective cause.

Back to the study itself, though…

What they found, and how they found it

Researchers took pancreatic islets from 140 heterogenous donors (varied in age and sex; ostensibly mostly non-diabetic donors, but they acknowledge type 2 diabetes could potentially have gone undiagnosed in some donors*) and tested cell cultures from each with various carbs, proteins, and fats.

They found the expected results in most of the cases, but around 9% responded more strongly to the fats than the carbs (even more strongly than to glucose specifically), and even more surprisingly 8% responded more strongly to the proteins.

*there were also some known type 2 diabetics amongst the donors; as expected, those had a poor insulin response to glucose, but their insulin response to proteins and fats were largely unaffected.

What this means

While this is, in essence, a pilot study (the researchers called for larger and more varied studies, as well as in vivo human studies), the implications so far are important:

It appears that, for a minority of people, a lot of (generally considered very good) antidiabetic advice may not be working in the way previously understood. They’re going to (for example) put fat on their carbs to reduce the blood sugar spike, which will technically still work, but the insulin response is going to be briefly spiked anyway, because of the fats, which very insulin response is what will lower the blood sugars.

In practical terms, there’s not a lot we can do about this at home just yet—even continuous glucose monitors won’t tell us precisely, because they’re monitoring glucose, not the insulin response. We could probably measure everything and do some math and work out what our insulin response has been like based on the pace of change in blood sugar levels (which won’t decrease without insulin to allow such), but even that is at best grounds for a hypothesis for now.

Hopefully, more publicly-available tests will be developed soon, enabling us all to know our “insulin response type” per the proteome predictors discovered in this study, rather than having to just blindly bet on it being “normal”.

Ironically, this very response may have hidden itself for a while—if taking fats raised insulin response without raising blood sugar levels, then if blood sugar levels are the only thing being measured, all we’ll see is “took fats at dinner; blood sugars returned to normal more quickly than when taking carbs without fats”.

You can read the study in full here:

Proteomic predictors of individualized nutrient-specific insulin secretion in health and disease

Want to know more about blood sugar management?

You might like to catch up on:

• 10 Ways To Balance Your Blood Sugars
• Track Your Blood Sugars For Better Personalized Health
• How To Turn Back The Clock On Insulin Resistance

Take care!

Which Osteoporosis Medication, If Any, Is Right For You?

We’ve written about osteoporosis before, so here’s a quick recap first in case you missed these:

• The Bare-bones Truth About Osteoporosis
• Exercises To Do (And Exercises To Avoid) If You Have Osteoporosis
• We Are Such Stuff As Fish Are Made Of
• Vit D + Calcium: Too Much Of A Good Thing?

All of those look and diet and/or exercise, with “diet” including supplementation. But what of medications?

So many choices (not all of them right for everyone)

The UK’s Royal Osteoporosis Society says of the very many osteoporosis meds available:

❝In terms of effectiveness, they all reduce your risk of broken bones by roughly the same amount.

Which treatment is right for you will depend on a number of things.❞

…before then going on to list a pageful of things it will depend on, and giving no specific information about what prescriptions or proscriptions may be made based on those factors.

Source: Royal Osteoporosis Society | Which medication should I take?

We’ll try to do better than that here, though we have less space. So let’s get down to it…

First line drug offerings

After diet/supplementation and (if applicable) hormones, the first line of actual drug offerings are generally biphosphates.

Biphosphates work by slowing down your osteoclasts—the cells that break down your bones. They may sound like terrible things to have in the body at all, but remember, your body is always rebuilding itself and destruction is a necessary act to facilitate creation. However, sometimes things can get out of balance, and biphosphates help tip things back into balance.

Common biphosphates include Alendronate/Fosamax, Risedronate/Actonel, Ibandronate/Boniva, and Zolendronic acid/Reclast.

A common downside is that they aren’t absorbed well by the stomach (despite being mostly oral administration, though IV versions exist too) and can cause heartburn / general stomach upset.

An uncommon downside is that messing with the body’s ability to break down bones can cause bones to be rebuilt-in-place slightly incorrectly, which can—paradoxically—cause fractures. But that’s rare and is more common if the drugs are taken in much higher doses (as for bone cancer rather than osteoporosis).

Bone-builders

If you already have low bone density (so you’re fighting to rebuild your bones, not just slow deterioration), then you may need more of a boost.

Bone-building medications include Teriparatide/Forteo, Abaloparatide/Tymlos, and Romosozumab/Evenity.

These are usually given by injection, usually for a course of one or two years.

Once the bone has been built up, it’ll probably be recommended that you switch to a biphosphate or other bone-stabilizing medication.

Estrogen-like effects, without estrogen

If your osteoporosis (or osteoporosis risk) comes from being post-menopausal, estrogen is a very common (and effective!) prescription. However, some people may wish to avoid it, if for example you have a heightened breast cancer risk, which estrogen can exacerbate.

So, medications that have estrogen-like effects post-menopause, but without actually increasing estrogen levels, include: Raloxifene/Evista, and also all the meds we mentioned in the bone-building category above.

Raloxifene/Evista specifically mimics the action of estrogen on bones, while at the same time blocking the effect of estrogen on other tissues.

Learn more…

Want a more thorough grounding than we have room for here? You might find the following resource useful:

List of 82 Osteoporosis Medications Compared (this has a big table which is sortable by various variables)

Take care!