In the quest to manage and mitigate various health conditions, the medical community often relies on potent pharmaceuticals like steroids, antipsychotics, statins, diuretics, and beta blockers. These drugs, while providing critical therapeutic benefits, also carry a lesser-known risk: the induction of Type 2 diabetes.
As the incidence of diabetes continues to rise globally, understanding the connection between these commonly prescribed medications and the onset of diabetes is paramount. These drugs can alter metabolic processes, leading to insulin resistance and heightened blood sugar levels, often culminating in a diagnosis of Type 2 diabetes.
That said, it is also essential to recognize that medications are not the sole contributors to the development of diabetes. Four primary non-pharmaceutical factors also play a significant role in its induction: excessive intake of linoleic acid, estrogen dominance, exposure to electromagnetic fields (EMFs), and the resultant endotoxin production in your gut. Each of these elements can disrupt your body’s metabolic balance and insulin regulation, paving the way for diabetes.
The Serious Fallout From Corticosteroid Use
High-dose corticosteroids are a common medical intervention. The most common and worst way to treat arthritis, steroids work by inhibiting the production of inflammatory chemicals. First synthesized in the 1930s, by the 1950s they were commonly used for to joint pain.1 Steroids have been recommended for the treatment of autoimmune disorders since the early 1980s, as a method of stopping the inflammation.2
Unfortunately, the harmful side effects of steroids are impossible to miss. Many of the most damaging and toxic effects of steroids had been by identified by 1960s, with elaborate protocols of lowering steroid dosages and withdrawing were developed to minimize the damage.3 But there is no hiding the dramatic impact these drugs can have after even short-term use.
Notable effects of corticosteroids include osteoporosis, cataracts and hyperglycemia. Studies have shown they are no better than a placebo for knee pain while doubling cartilage loss.4
The immune suppressing abilities of steroids which led to them being used to treat autoimmune diseases in the first place also leaves patients vulnerable to sepsis and infection.5 Fluid buildup, behavioral changes, weight gain, fatigue, muscle weakness and increased risk of infection from common virus and bacteria are other common issues associated with medical steroid use.6
Steroid Induced Diabetes
With such an extensive list of potential health problems resulting from corticosteroid use, steroid induced high blood sugar and diabetes might be the most pervasive and common issue. In a hospital setting, more than half of patients receiving high-dose steroids develop hyperglycemia and a full 86% encounter at least one episode.7
Diabetes is an insulin resistance disease that results in high blood sugar. Your pancreas produces insulin, which is the hormone that controls blood sugar levels.8 Corticosteroids induce diabetes by making your liver more resistant to insulin. So, even if your pancreas is producing sufficient insulin, your liver continues to produce glucose.
Steroids are a significant cause of post-meal hyperglycemia and insulin therapy coincident with meals is the typical treatment.9 Globally, oral corticosteroids are linked to 2% of new cases of diabetes.10
One of the most alarming aspects of steroid induced diabetes is how quickly it occurs. Blood glucose levels have been shown to spike the day after steroid injections for musculoskeletal pain.11 Steroid induced diabetes is not always permanent, but it’s a possibility if you are at risk of Type 2 diabetes.12
Antipsychotic Agents
A healthy lifestyle that reduces the toll of aging is the best approach to avoiding corticosteroids, the use of which makes hyperglycemia almost unavoidable. Commonly prescribed second-generation antipsychotic drugs are also associated with diabetes.
Clozapine-induced prediabetes and diabetes was found in 76.52% of patients in one study, with the addition of metformin failing check progress to diabetes in 47% of the prediabetes patients.13
A Danish cohort study found second generation antipsychotics increased the risk of developing diabetes by 32%, with the risk being 24% higher still with risperidone.14 It occurs at an alarming pace, generally within six months of initiation.15
Weight gain and new onset diabetes are serious drawbacks to second-generation antipsychotics. Forty percent of patients taking olanzapine encountered significant weight gain but researchers did not find the weight gain to be associated with diabetes. This failure to understand the underlying metabolic disturbances shifts the emphasis for treatment. Behavioral treatments and additional medications only have had limited clinical success in reversing these adverse effects.16
Diabetes From Commonly Prescribed Cholesterol, Blood Pressure and Heart Medications
Statins are among the most commonly prescribed drugs. Their popularity is driven more by drug industry profit than need, as millions at low risk for cardiovascular disease are prescribed this class of drug. The statin empire has been built on sales techniques and changing cholesterol guidelines. Lipitor, made by VIATRIS, has been prescribed to over 29 million patients.17
Statins double diabetes rates and if taken for more than three years can triple your risk. They are a clumsy tool and work by blocking an enzyme in the liver that your body uses to make cholesterol. This sounds simple enough, except your body is complex and changing one factor can cause unintended or adverse events.
Rather than adopting lifestyle strategies to improve health holistically, the conventional solution to the diabetes and statin link is yet another drug. Glyburide is an oral diabetes medicine with its own list of adverse effects. These include liver damage, nausea, heartburn, blurred vision, muscle and joint pain.18
A journalist at Diabetes.co.uk pointed out how strange this statin-glyburide prescription chain is, stating, “As glyburide stimulates insulin production, using a Type 2 diabetes drug to prevent Type 2 diabetes seems a peculiar treatment.”19
Thiazide diuretics, another popular class of drug used to treat hypertension, also have a deserved association with new onset diabetes. Thiazide diuretics decrease sodium reabsorption and increase urine flow, literally draining and reducing the intercellular and plasma volume from cells.20 Analysis has shown that patients receiving this class of drug have higher risk of impaired glucose tolerance and diabetes.21
Protecting cardiovascular health is also the purpose of beta blockers. They are prescribed to manage abnormal heart rhythms. They work by blocking the production of adrenaline. This results in a heart that beats slower and with less force. They also widen veins and arteries to improve blood flow and reduce blood pressure.22
Naturally, there is fallout from this type of intervention. Beta blockers can raise the risk of Type 2 diabetes by reducing insulin sensitivity.23 In insulin dependent diabetics, beta blockers can prolong, enhance, alter and worsen symptoms of hypoglycemia or low blood sugar.24 The opposite is the case if you are a non-insulin dependent diabetic.
Then hyperglycemia becomes a major risk. Beta blockers antagonize the action of oral hypoglycemic drugs and can increase blood glucose concentrations.
Avoiding and Recovering From Medication Induced Diabetes by Avoiding PUFAs
The side effects of these common drugs are alarming, with new onset diabetes being especially common. Your best bet is to pursue a lifestyle that removes the use of these prescriptions from the table. As hinted at earlier, the surge in chronic diseases that these diabetes-promoting drugs are used to treat can be traced to three pervasive mitochondrial poisons: linoleic acid, estrogen dominance and EMFs.
Virtually every disease known to man, including the major one like heart disease, cancer and obesity, are linked to compromised cellular energy production, brought on by these toxins, which create a gut environment where endotoxin-producing bacteria thrive.
So, the primary objective for any illness is to first reestablish healthy energy production, which will allow your body to keep your large intestine free of oxygen. That will then facilitate the restoration of your normal gut flora. The key here is that the inability to exclude oxygen from your large intestine, where it’s not supposed to be, is directly linked to inadequate energy production.
Maximize Your Mitochondrial Function Optimal Health
Like many, I used to believe glucose was an inferior fuel to dietary fat, when in fact it’s the complete opposite. Similarly, while many understand that processed foods aren’t good for you, most lay the blame on sugar, when in fact it’s the seed oils that do most of the harm. Excess linoleic acid and estrogen dominance are the major contributors to mitochondrial disfunction.
Sure, refined sugar in high amounts is not healthy, but even refined sugar isn’t as bad as polyunsaturated fats (PUFAs) and to a slightly lesser degree, monounsaturated fats (MUFAs). So, eliminating seed oils is a key strategy for optimal health.
As explained in far greater detail in previous articles, if you eat too much dietary fat, your body ends up favoring fat metabolism at the expense of glucose metabolism, and burning glucose in your mitochondria is the pathway that creates the greatest energy production. So, excessive fat intake actually results in suboptimal energy production.
Industrial mitochondrial toxins such as omega-6 fats from vegetable and seed oils, estrogens, plastics with estrogen-like additives, and electromagnetic fields (EMFs), severely impact energy production in your mitochondria.
This reduction in energy is crucial because every process in your body relies on sufficient energy availability; when it’s lacking, your overall health will deteriorate. By increasing your mitochondrial energy production, you will typically have the ability to avoid prescription drugs entirely.
Analysis by Dr. Joseph Mercola
Sources & Resources
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2 Hospital Practice, 1983 October;18(10):99-103, 107-18, 113-4, Abstract
4 JAMA 2017; 317 (19): 1967-1975
5 Mayo Clinic, Prednisone and other corticosteroids, How do corticosteroids work?
6 Mayo Clinic, Prednisone and other corticosteroids, Side effects of corticosteroids taken by mouth
7 World Journal of Diabetes, 2015 Jul 25; 6(8): 1073-1081, Epidemiology and Risk Factors
8 National Institute of Diabetes and Digestive and Kidney Disease, Insulin Resistance and Prediabetes, What is insulin
9 Diabetes/Metabolism Research and Reviews, 2014 Feb; 30(2): 96-102, Summary
10 Diabetes Journal, 2006 December, Issue 12, Conclusions
11 Annals in Rehabilitation Medicine, 2020 Apr; 44(2): 117-124, Methods
12 Diabetes.org.uk, Is steroid-induced diabetes permanent?
13 Journal of Affective Disorders, 2021 Dec 1:295:163-172, Results
14, 15 Endocrinology, Diabetes & Metabolism Case Reports, 2018; 2018: 18-003, Background
16 Journal of General Internal Medicine, 2004 Dec; 19(12): 1200-1205, Discussion
17 About Lipitor, Why Lipitor
18 Drugs.com, Glyburide, Glyburide side effects
19 Diabetes.co.UK, 2015 June 23
20 Drugs.com, Thiazide diuretics
21 Journal of the American Society of Nephrology, 2004 November, 15(11):2948-2950
22 Drugs.com, Beta blockers
23 Diabetes.co.uk, Drug Induced Diabetes
24 Drug Intelligence and Clinical Pharmacy, 1985 Apri;19(4): 246-51, Abstract