The real culprit behind post-holiday depression

And the simple key to reclaiming your happiness—through the winter and beyond  

The New Year has arrived. And the party’s over, so to speak. After six weeks of celebrating with family and friends, it’s back to the daily grind again. There are bills to pay and decorations to put away—not to mention the bitter cold and long nights to contend with. It’s enough to depress just about anyone…

But for some people, the struggle over the next few months is particularly intense—and it’s not hard to see why. The post-holiday period can often be a disastrous recipe for weighing down your mental health. 

Shorter days can spark seasonal affective disorder (SAD) and steal your best source of vitamin D, the sun—two wintertime risk factors that most depression-prone patients already have on their radars. (I’ve covered this topic in detail here before, most notably back in the November 2013 issue.) 

But there’s one more complication you might not have considered—at least, not as a direct threat to mental health. And while I’ve addressed this particular subject many times before (even in this very issue), this is the first time I’ve delved into the role it plays in depression. 

If you haven’t already guessed, I’m talking about inflammation. Why? Because the latest research suggests that its impact on your mood is very real. And incredibly dangerous, too. 

When physical illness becomes mental illness 

The idea that neuroinflammation is the primary cause of depression is gaining traction with each new study on the subject. At the very least, it’s clear that the brain’s immune responses play a key biological role. 

Additionally, studies show that depressed patients have higher levels of pro-inflammatory cytokines. (Cytokines are proteins vital in cell-to-cell communication and protecting the immune system.) And studies have also shown that inflammatory drug therapies—for example, 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 no wonder: 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, too. 

In fact, one 2016 study published in the Journal of Clinical Psychiatry revealed that levels of patients’ C-reactive protein—a key inflammatory biomarker typically associated with cardiovascular disease—were 31 percent higher in depressed patients, as 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, in these depressed patients, 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 

I’m always telling you that inflammation is the root of all disease. And as this research shows, the brain is hardly off limits. Depression—much like Alzheimer’s and Parkinson’s, two neurodegenerative diseases in which brain inflammation also plays a role—is just another example of its insidious influence. 

You can see, now, why extra sunshine won’t always do the trick when you’re struggling. (And don’t even get me started on antidepressant drugs, which are both risky and ineffective in many patients.) 

But anti-inflammatory drugs—which these researchers predictably cited as a potential solution—aren’t the answer, either. Because the fact is, you don’t need drugs (of any kind) to extinguish chronic inflammation. You only need to commit to a few key lifestyle changes. 

Generally speaking, this means being mindful of your nutrition, sleep, and exercise habits. (All of which may have taken a backseat through the busy holiday season.) You should also know there’s one strategy that’s particularly effective at combating brain inflammation.

A ketogenic diet brings your brain back from the brink

You might recall that 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 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. 

The use of a ketogenic diet as an epilepsy treatment dates all the way back to the 1920s. And while it was largely sidelined with the advent of anti-seizure drugs, this approach has seen a resurgence over the last couple of decades. (Primarily due to the fact that, unlike drugs, the ketogenic diet is both safe and free of side effects.) 

But this renaissance has also introduced a long list of completely new applications—with research investigating the potential role of ketogenic diets in combating everything from cancer to Alzheimer’s disease. (In fact the research on its role in cognitive decline is so compelling, I based an entire lesson on it in my brand new Drug-Free Protocol for Reversing Alzheimer’s and Dementia. You can learn more about it—or enroll today—using the details I mentioned on page 5.

And considering the effects that ketosis has on the body’s inflammatory response (and on neuroinflammation in particular), it’s about time.  

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.4 

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 something as seemingly unrelated as depression. 

Especially since ketosis is actually much more attainable than the naysayers (and mainstream medicine is full of them) would ever lead you to believe.  

Two simple ways to maintain ketosis for life

I outlined the basics of ketogenic dieting back in the May 2017 issue (which you can access from the archives by logging into the “Subscriber” section of with your username and password). But the first—and most important—step is to cut out carbohydrates. Yes, even the so-called “healthy” ones.

Cutting carbs is the only way to ensure your body taps into fat stores for energy. Otherwise it will “default” to using the glucose created when your body breaks down carbs. Admittedly, the first few days will probably be a challenge, especially if you’re used to eating a lot of carbs. 

But by the end of the first week, you’ll start to notice a big difference in how you feel. And by the end of the second week, your energy levels, mental clarity, and weight loss will all be kicked into high gear. 

In fact, my patients who follow ketogenic diets insist they feel stronger and sharper than they ever have. And that’s certainly been my experience, too.

Of course, carb restriction isn’t the only strategy that will help you to achieve ketosis. Intermittent fasting (IF)—where you restrict all calorie intake, for regular periods of 16 to 24 hours at a time—can get you there, too. 

This may sound off-putting. But IF has been gaining a lot of attention in research circles, in part because its payoff is so big… and it’s not nearly as hard to manage as it sounds. In fact, this is how I eat. I’ve eaten only one meal a day for most of the past decade, and I feel great.

And if you think about it, it’s how we were genetically programmed to eat. We didn’t evolve with refrigerators. Initially, we had to hunt for our food, and there’d be many hours of the day we’d go without food.

Granted, fasting is not for everyone. But there’s growing evidence that ketosis is something we all should strive for—whether you struggle with depression or not.


  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. Shen Y, et al. Nat Commun. 2017 Sep 22;8(1):624.