Chiropractic Wellness Center Ltd

07/25/2026

One cannot overestimate the value of heat and cold therapy! Cool history story here!

Of all the injuries or illnesses suffered throughout the Expedition, William Bratton’s was one of the worst. While assigned to the Salt Camp on the Pacific coast during the winter of 1805-06, about 15 miles from Fort Clatsop, Bratton suffered an injury that was nearly debilitating – severe low-back pain. Even today, it is often a malady that is difficult to diagnose and even harder to cure without surgery. And surgery for such this type of injury in the early 19th century was unheard of.

Bratton’s pain would continue for months and became so severe that he found it difficult to sit up, and impossible to walk. The Captains gave him huge doses of Peruvian (chichona) bark (which contains quinine) and laxatives, but these treatments seemed to do nothing.

In March 1806, when the Corps started paddling up the Columbia River, the private’s back appeared to have improved. But it was only temporary. By April 11, Meriwether Lewis noted that Bratton “...is yet so weak he is unable to work... .” By April 20, when the party prepared to tackle the Rocky Mountains on horseback, the pain grew worse and Lewis provided an update: “Bratton was compelled to ride as he was yet unable to walk.”

When the Corps stopped to rest in mid-May with the Nez Perce, near today’s Kamiah, Idaho, John Shields suggested an idea that he hoped would help his ailing colleague and friend. The blacksmith sunk a circular hole about three feet in diameter and four feet deep into the earth. After building a sizable fire to heat the hole for a period of time, he quickly removed the ashes. Then a willow branch hoop, covered with blankets, was placed over the hole and Bratton was stripped naked and carried inside. After 20 minutes, he was removed and plunged into a cold stream. This was repeated.

Amazingly, Bratton felt almost immediate improvement. William Clark wrote the next day, “bratten is walking about to day and is much better than he has been.” By June 8, Lewis declared, “we cannot well consider him an invalid any longer.” The Corps’ version of an Indian sweat lodge seemed to be the cure – an alternating hot and cold physical therapy treatment still practiced today.

Image: Shield’s miniature sweat lodge would have been similar to this Nez Perce sweat lodge, photographed in about 1910 by Edward S. Curtis. Within the Curtis Collection, Library of Congress.

Image Description: A black-and-white photograph shows a small domed structure in the foreground, partially covered with a dark blanket. It stands in a rocky valley with several grass-covered hills in the background.

07/25/2026

Do you know your Apolipoprotein B levels (Apo B)? You should! Much more important than your LDL numbers!

🚨 Your LDL cholesterol can look perfectly normal while hundreds of dangerous particles silently pack your arteries with plaque.

This is the mistake that sends people with "good" cholesterol numbers to the cardiac catheterization lab every single day.

But the data says otherwise, and ApoB is the number that actually tells the truth.

And no, this is not just a niche lab test for cardiology nerds.

🫀 What is ApoB and why does it matter?

ApoB stands for apolipoprotein B. It is the structural protein that sits on the surface of every single atherogenic particle in your blood. Every LDL particle carries exactly one ApoB molecule. Every VLDL particle carries exactly one ApoB molecule. Every IDL particle carries exactly one ApoB molecule. Every Lp(a) particle carries exactly one ApoB molecule.

That one-to-one relationship is the entire point.

When you measure ApoB, you are counting the actual number of dangerous particles in your blood. Not the cholesterol weight stuffed inside them. The particles themselves.

🔬 Here is what the science actually says.

Plaque does not build because cholesterol is heavy. Plaque builds because particles enter the artery wall and get trapped there. Once trapped, the immune system attacks them, foam cells form, and the atherosclerotic lesion begins. The number of particles determines how often that trapping happens. A high particle count means more chances for a particle to lodge in the endothelium and start that process.

LDL cholesterol measures cargo weight, not particle count.

Two people can have identical LDL cholesterol numbers. One person has 900 large, buoyant LDL particles. The other has 1,400 small, dense LDL particles. The second person has 56% more atherogenic particles in circulation. Their ApoB tells you that. Their LDL does not.

That is the real story.

🩺 I am a board-certified cardiologist and the founder of a preventive cardiology practice.

I have seen this pattern hundreds of times in my clinic. A patient walks in with an LDL of 95, which looks reassuring on paper. Their ApoB comes back at 118 mg/dL. That is elevated. That is residual risk sitting in plain sight, invisible to the standard lipid panel. We would have missed it entirely if we stopped at LDL.

This is why every patient who comes through my doors gets an ApoB measured.

⚠️ The LDL problem runs even deeper when triglycerides enter the picture.

When your triglycerides are high, your blood fills with VLDL particles. VLDL particles carry ApoB too, and they are atherogenic. But your standard lipid panel does not count them as particles. It estimates LDL cholesterol using a formula that actually becomes less accurate as triglycerides rise. Above a triglyceride level of 400 mg/dL, the standard LDL calculation is so unreliable that labs will not even report it.

ApoB captures VLDL. ApoB captures IDL. ApoB captures Lp(a).

One number. Every dangerous particle. No estimation.

💓 The trial data backs this up.

✅ The INTERHEART study: ApoB to ApoA1 ratio outperformed every other lipid measure as a predictor of heart attack risk across 52 countries.

✅ The AMORIS study: ApoB predicted cardiovascular events more accurately than LDL cholesterol in a population of 175,553 patients.

✅ The 2026 ACC/AHA lipid guidelines now formally recognize ApoB as a preferred marker for cardiovascular risk assessment. That is not a suggestion from the fringe. That is the mainstream guideline finally catching up to the data.

🔸 What is a normal ApoB level?

For most people, the target is below 100 mg/dL.

For high-risk patients, including those with established heart disease, diabetes, or multiple risk factors, the target drops to below 80 mg/dL.

For very high-risk patients, some guidelines now push toward below 70 mg/dL.

Your standard cholesterol panel will not tell you where you stand on any of these targets.

👤 Let me give you a real-world picture.

A patient who knows their ApoB, works with their cardiologist to drive it below 80 mg/dL, and sustains that target through lifestyle and medication can halt plaque progression and in some cases reverse early atherosclerosis within 12 to 24 months.

A patient who only tracks LDL and celebrates a number of 95 mg/dL may spend that same 12 to 24 months building silent plaque with an ApoB of 115 mg/dL.

That is the difference between stopping the disease and discovering it on a cath table.

❌ Knowing your LDL alone is not enough.
❌ A "normal" LDL is not the same as a safe particle count.
❌ Your standard lipid panel is not showing you the whole picture.

"The question is no longer what is your LDL. The question is how many atherogenic particles are in your blood right now."

❤️ Bottom line:

ApoB is not a specialty test for complicated patients. It is the most precise lipid measurement available to every person who wants to know their true heart attack risk. It counts every dangerous particle. It catches what LDL misses. It is supported by data from hundreds of thousands of patients and now endorsed by the 2026 guidelines. Ask your doctor for your ApoB number at your next visit. If it is above 100 mg/dL, that is a conversation worth having. If your doctor does not know what to do with it, find one who does.

Are you monitoring your ApoB or are you still flying blind on LDL alone?

Comment "blog" and I will send you the link.

05/25/2026

So valuable!

A researcher in Australia asked a question that got her laughed out of the room: could what we eat be one of the biggest drivers of depression?

So she ran the first randomized controlled trial ever designed to test whether changing diet could treat clinical depression. One group got dietitian support. The other got friendly social visits. Same amount of contact. Same amount of attention.

After 12 weeks, 32 percent of the diet group no longer met the criteria for depression. The social support group? Eight percent.

Food wasn't just important for health. It was treatment.

The science behind it is straightforward. Your gut is lined with trillions of microbes that make the building blocks for serotonin and dopamine. Ultra-processed foods destroy those microbes and trigger chronic inflammation. That inflammation disrupts your brain's wiring, shrinks the hippocampus, and locks your stress response in the on position.

Diets rich in fiber, whole plants, and fermented foods do the opposite. They rebuild the gut, calm the inflammation, and give your brain the raw materials it needs to regulate mood.

Ultra-processed foods now make up 58 percent of the average American's calories. Depression is the number one cause of disability worldwide. These two facts are not unrelated.

You don't need a complete overhaul. Even a 20 percent improvement in diet quality significantly lowers depression and anxiety risk. Add two vegetables at lunch. Eat beans three times this week. Put a jar of sauerkraut in your fridge.

Your plate is either building serotonin or burning it down. Every bite is a message to your brain.

I wrote a full article on the science of nutritional psychiatry, plus a 7-Day Mood Food Reset Worksheet with a plant diversity tracker, daily habits tracker, and meal framework.

Read it below 👇️

Share this with someone who's been struggling with mood and has never considered that the answer might be on their plate.

05/25/2026

Happy Memorial Day!

05/17/2026

How do I tell my Dad Roundup is bad, hard to argue with an 89 yo.... But we should avoid it.....

Cancer is not the only health risk associated with glyphosate exposure.

For years, it was argued that because glyphosate kills plants through a metabolic pathway called the shikimate pathway, it is safe for humans since we do not have this pathway. However, our gut bacteria DO have this pathway!

To reduce glyphosate exposure and minimize the consumption of toxic chemicals in your food, do the following:

1. Opt for organic when possible.

2. Replace cereals with a protein breakfast.

3. Support gut health with fermented foods.

4. Test urine for glyphosate levels.

Find out more about how they’re poisoning Americans: https://drbrg.co/4nveVSj

Dr. Eric Berg, DC, not MD; information only

04/04/2026

04/04/2026

Maltodextrin.... Do you ever read your food labels? Check out the Yuka app for your smart phone. Just scan the barcode on a product and get instant feedback on great, good, bad etc. And it will tell you why! Too much salt, sugar, bad fat, etc as well as additives and if they are really bad or just so-so.

04/03/2026

Too good not to share...... I enjoy being a chiropractor and helping others! But we all need to remember, there is no magic quick fix for many health problems. Chiropractic adjustments are a great natural approach for many conditions, there is even a time for medications, injections, surgery, etc. But if we are not willing to help ourselves, make a few positive lifestyle changes, our improvements with many treatments are often going to be somewhat limited and possibly short lived.

04/01/2026

If you want to live a long and healthy life, it is essential to tend to your inner garden: the microbiome.

04/01/2026

Interesting! This is the principle of hormesis. The same principle behind why exercise works (muscle damage triggers repair and growth), why sauna exposure improves cardiovascular health (heat stress triggers protective adaptations), and why fasting has metabolic benefits (nutrient scarcity activates cellular cleanup).

People who live at higher elevations have consistently lower rates of type 2 diabetes. This has been observed across multiple countries, cultures, and lifestyles. For years, researchers assumed it was lifestyle differences. More walking. Less processed food. Thinner air forcing the body to adapt.

But new research has identified the actual biological mechanism, and it is more interesting than anyone expected.

At high altitude, the body adapts to lower oxygen availability. This triggers a cascade of metabolic changes that improve how cells handle glucose. The adaptations mimic some of the same pathways that are activated by exercise and caloric restriction, two of the most well-established interventions for metabolic health.

In other words, the stress of altitude does something useful. It forces the body into a state of mild metabolic challenge, and the body responds by becoming more efficient.

This is the principle of hormesis. The same principle behind why exercise works (muscle damage triggers repair and growth), why sauna exposure improves cardiovascular health (heat stress triggers protective adaptations), and why fasting has metabolic benefits (nutrient scarcity activates cellular cleanup).

For those of us living at sea level, the lesson is not to move to the mountains. It is that mild, voluntary stress is medicine. The body does not get stronger from comfort. It gets stronger from challenge.

A brisk walk. A cold rinse at the end of a shower. A meal with a longer gap between the last one. A 3-second eccentric chair lower. These are all sea-level versions of altitude.

Challenge your body gently. It was built for it.