Two devastating effects of chronic inflammation— and one simple way to protect yourself

I talk about inflammation a lot. After all, ongoing, systemic inflammation can do a real number on your body. In fact, it’s the root cause of most illnesses—including a few you might not expect.

Case in point: It’s easy to think of your mind and your body as being two completely separate entities. But the truth is, your brain is just as susceptible to the insidious effects of inflammation—and its impact on everything from your memory to your mood can be nothing short of devastating…

A hidden source of depression

While we tend to think of clinical depression as an emotional concern, inflammation in the brain appears to be one driving factor behind this diagnosis. And it’s clear that the brain’s immune responses play a key biological role in the development of this condition.

Fortunately, the idea of neuroinflammation as a primary cause is gaining more and more traction. For one thing, studies show that depressed patients have higher levels of pro-inflammatory cytokines. (Cytokines are vital proteins in cell-to-cell communication and protecting the immune system.)

Studies have also shown that inflammatory drug therapies—like interferon treatment (injecting cytokines to help the body fight off virus infections)—trigger depression in as many as half of all patients.

And it’s really no wonder why: We now know that cytokines can interfere with a long list of key neurological processes—including neurotransmitter metabolism, brain hormone function, neuroplasticity, and behavior.1

This helps explain why stress—which also contributes to inflammation in the nervous system—often leads directly to depression. And why rates of depression are so much higher in patients with chronic inflammatory conditions like heart disease and arthritis.

In fact, one 2016 study published in the Journal of Clinical Psychiatry revealed that levels of patients’ C-reactive protein (CRP)—a key inflammatory biomarker typically associated with cardiovascular disease—were 31 percent higher in depressed patients, compared to their non-depressed counterparts.2

Another recent study assessed inflammation levels in 14 patients with untreated moderate-to-severe depression. More specifically, researchers used brain imaging to measure the activation of brain-specific immune cells called microglia. (These cells are your nervous system’s first and primary immune defense—responsible for clearing out toxins, dead neurons, and other cellular debris.)

Results revealed that microglial activation was centered in the area of the brain responsible for mood regulation. And this activation was particularly prominent among suicidal patients with major depression.3

A smoking gun behind dementia, too

None of this is particularly surprising when you consider the fact that research has revealed a lot of the same inflammatory mechanisms behind cognitive decline—and in Alzheimer’s disease (AD), in particular.

For example, we know that people with a gene called ApoE4 are at higher risk of AD—but that not all carriers go on to develop AD. Research suggests, however, that chronic inflammation lights the match.

Boston University researchers used data from participants of the Framingham Heart Study. And they found that, when subjects with the ApoE4 gene had chronic low-grade inflammation—in this case, defined by elevated CRP levels—they were also far more likely to wind up with dementia down the road.4

This suggests there would be no difference in Alzheimer’s risk between people with and without this notorious gene if chronic inflammation wasn’t there fanning the flames.

Other research has shown that, like depression, microglial activation in the brain plays a role in Alzheimer’s, too—and more recent research suggests that neuroinflammation may actually play a wider role in dementia than we realized, contributing to a number of other forms of the condition.5-6

Bottom line? Excess inflammation is your body’s way of telling you that something isn’t quite right. And as this research shows, it can grease the wheels of a vicious mind-body cycle. That’s why it’s as important as ever to start reining in some of the inflammation you may be experiencing—the right way.

One “solution” you can skip

A few years back, researchers in Vancouver completed studies that indicated ibuprofen—yes, one of the most popular over-the-counter, non-steroidal anti-inflammatory drugs (NSAID)—might be able to prevent AD if you start taking it early enough.7

But before you jump on the bandwagon, let’s take a closer look…

There’s no question that inflammation spells trouble for your cognitive health. But the real issue with this research is… why ibuprofen?

Sure, it may be a staple in medicine cabinets everywhere. But this drug is a known liver toxin, a cause of gastritis and ulcers, and ultimately comes with a list of side effects a mile long.

So, in my view, it’s best that you skip the ibuprofen—along with any other anti-inflammatory drug, for that matter—and turn to a safer, more effective route.

Extinguish the flames of inflammation at the source

As I’ve shared many times before, I got my start working alongside Dr. Robert Atkins, who made the high-fat, low-carb ketogenic diet famous. The main idea behind this diet is to achieve ketosis—where you switch your body’s main source of energy from sugar to alternative fuels called ketones (which your body forms by breaking down fat).

It’s an approach that’s fallen in and out of favor over the decades. But its neurological benefit, at least, has always been widely acknowledged. And considering the effects that ketosis has on the body’s inflammatory response (and on neuroinflammation in particular), it’s no wonder.

In fact, recent lab experiments from a team of scientists at The University of California, San Francisco found that inducing a ketogenic state can bring brain inflammation down to nearly optimal levels—delivering a much larger reduction than they had anticipated.8 

Of course, the main purpose of this research was to help identify strategies to reduce neuroinflammation in the critical time period following a brain injury. But it’s not hard to see the bigger picture here—even for issues as seemingly unrelated as depression or dementia.

The good news is, ketosis is actually much more attainable than many people seem to believe.(Not convinced? Order yourself a copy of my A-List Diet book—a Mediterranean-style, ketogenic eating guide—online at AListDietBook.com, and see for yourself!)

But for now, let me get back to the bigger point of this discussion… which is that inflammation poses a bigger threat to your health than just arthritis, cancer, heart disease, depression, or even AD.

In fact, there really isn’t a health problem out there that it doesn’t have a hand in. And that’s exactly why I developed my latest protocol, my Essential Guide to Combatting Inflammation.

This comprehensive, online learning tool will show you how to fight this stealth culprit behind premature aging, chronic pain, and deadly disease—safely and naturally. To learn more, or to enroll today, click here or call 1-866-747-9421 and ask for order code EOV3X502.

References:  

  1. Raison CL, et al. Trends Immunol. 2006 Jan;27(1):24-31. 
  2. Cepeda MS, et al. J Clin Psychiatry. 2016 Dec;77(12):1666-1671. 
  3. Holmes SE, et al. Biol Psychiatry. 2018 Jan 1;83(1):61-69.
  4. QiushanTao et al. Association of Chronic Low-grade Inflammation With Risk of Alzheimer Disease in ApoE4 CarriersJAMA Network Open, 2018 DOI: 10.1001/jamanetworkopen.2018.3597 
  5. FrikerLL, et al.  β-Amyloid Clustering around ASC Fibrils Boosts Its Toxicity in Microglia. Cell Reports, 2020; 30 (11): 3743 
  6. Rowe JB, et al.Neuroinflammation and protein aggregation co-localize across the frontotemporal dementia spectrumBrain, 2020; DOI: 10.1093/brain/awaa033 
  7. McGeerPLet alConquering Alzheimer’s Disease by Self TreatmentJournal of Alzheimer’s Disease, 2018; 1 DOI: 10.3233/JAD-179913 
  8. Shen Y, et al. NatCommun. 2017 Sep 22;8(1):624. 

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