Better with Age: The Science of Healthy Aging

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Better with Age: The Science of Healthy Aging

As you age, would you rather feel great, or look great? Why not both? 

A new perspective on aging may give you hope, regardless of whether you are 40 or 80.  Here’s why getting old does not just mean accepting the inevitable – wrinkles, gray hair, or cognitive decline. There is very advanced, albeit not highly publicized, technology in blood diagnostics that allows you to harness the good and work to minimize the bad, at least from a physiological standpoint. 

First, there are those that suggest we, as a culture, need to embrace aging with grace and acceptance. Of course. But that does not mean denying the reality that many age-related conditions can be treated, managed, or prevented. It goes without saying that we must at some point confront our mortality and the physical decline associated with it. A deeply personal and emotional issue, our mortality, and by extension, our aging years are influenced by a myriad of non-biological factors, many of which are beyond our control – geography, family, money, past decisions. 

That said, many biological factors are indeed capable of being manipulated, for better or worse, and a new approach to aging is gaining attention which is this: Whether you are 40 or 90, physical health begins in the cell.

What does this mean exactly?  If you are 40 years old, but your cells are dysfunctional, inefficient or damaged, the cell is acting “older” than it should.  It is aged.  Conversely, if you are 75 years old, but due to epigenetic “luck” (more on that later), or clean living, or a combination of both, your cells are humming along strong, adaptable and functioning well, then you may say your cells are acting “younger.”  The cumulative effect of these cells is healthier, functional tissue throughout the body, which ultimately manifests as a healthy person. 

In other words, healthy cells = healthy tissue = healthy humans, regardless of chronological age.  

But that begs the question of why cells become unhealthy and dysfunctional in the first place.  Why is seemingly every chronic condition – heart disease, high blood pressure, cancer, mental clarity, our waistlines – worse in the older age groups?  Reasons vary from person to person, of course, but here are two highly underappreciated, but highly modifiable factors that can profoundly influence how we age:

  1. Micronutrient deficiencies (particularly, their cumulative effect)
  2. Immune cell dysfunction

These are unequivocally related, directly and indirectly.  First and foremost, micronutrient deficiencies absolutely cause immune cell dysfunction.  If your immune cells lack a key vitamin or mineral (which varies by person), they will exhibit some form of cellular dysfunction. Cellular dysfunction means the cell cannot do its job.  For immune cells, their job is to adapt and protect, not just from pathogens like viruses and bacteria, but also from endogenous threats like tumor cells. 

The immune cell (specifically, we’re all talking about T-lymphocytes, aka T-cells) needs to adapt to the specific threat.  Sometimes T-cells need to kill an infected cell, sometimes T-cells need to reduce inflammation, sometimes T-cells need to create inflammation, often T-cells simply need to direct other immune cells, like an army general – it all depends on the specific physiological threat. Being adaptable is key to doing its job, which is to protect our biological tissues.

How do micronutrients fit in? 

Guess what the immune cells need to perform all the functions needed to protect us – you guessed it, MICRONUTRIENTS.  These are the tools, materials, helpers, signalers, regulators – that are needed for cell function.  Micronutrients are so fundamental to cell health that their functions often overlap. These redundant mechanisms are good because cells can compensate when a nutrient is missing.  But, over time, the compensatory mechanisms also falter depending on the degree and severity of nutrient deficiencies, as well as the person's own personal requirements.  This is the point where cell dysfunction starts to manifest as symptoms.

Before overt symptoms, which notably happen more often as we age, nutrient deficiencies usually exist sub-clinically, which means you do not see them manifest in obvious symptoms, at least at first.  But a dysfunctional cell, by definition, cannot function. If that dysfunctional cell is an immune cell, the “symptom” may be cancer cells that are not cleared from the body before they get out of control. Or, that “symptom” of a dysfunctional immune cell may be decreased immunity and all the sequelae that go with that. The underlying problem is cell dysfunction. The underlying cause is (more often than not) micronutrient deficiency.

What does this have to do with aging, you may ask?  Because the conditions of aging (loss of motility, cognitive decline, low energy, risk of infections, etc.) and the diseases of aging (heart disease, diabetes, cancer, dementia, arthritis, etc.) are all exacerbated, if not directly caused by, micronutrient deficiencies. Correct the deficiency, cells perform better. In this way, the diseases of aging can be thwarted.  Regardless of what the calendar says, if your cells are healthy, you will likely look and feel great. 

You may ask “what about genetics?”  Valid question, but the role of genetics is often wildly misunderstood.  In a gross simplification, we are not our genes.  It’s more accurate to say we are our ‘expressed’ genes, but this too is an oversimplification.  In reality, we are a culmination of the expression (or non-expression) of genes in our past, present, and future environments.  And by ‘environment’, we mean the physical, physiological, and emotional reality in which we find ourselves.  In other words, our genes are profoundly affected by our biological environment, which includes micronutrient status.

Let’s take the highly publicized biomarker for aging – telomeres.  These are bits of DNA at the ends of our chromosomes whose function is to protect the rest of our DNA from unraveling into a hot mess of genetic tangles. The commonly used analogy is an aglet, which is the formal name of the plastic on the ends of shoelaces that protect the lace from getting frayed. Telomeres are a chromosomal aglet.  Here’s how they work:  when a cell divides, a tiny portion of the tip of the chromosome (in the telomere region) is lost, and that chromosome is a wee bit shorter than before the cell division.  Once all the DNA in the telomere is lost (after subsequent cell divisions), the cell’s chromosome is “exposed” and can tangle or fray (like a shoelace without an aglet), and consequently, the cell dies.

Shorter telomeres = older cells. No more telomere = a cell is about to die.

Here’s where micronutrients come in once again. Guess what helps protect telomeres?  Micronutrients. Guess what degrades telomeres?  Micronutrient deficiencies. Various biologic mechanisms are at play but the bottom line is that poor nutrient status, at the cellular level, will shorten telomeres and lead to biological aging. Not all deficiencies will affect the same pathway since we are biochemically unique. That is why there is not one ‘magic pill’ that slows cellular aging. Your ‘magic pill’ will be different than someone else. 

The key is to find out what your actual cells need (in terms of micronutrients) and give it to them. 

Click here for a more complete list of micronutrients and how they affect telomeres. 

When it comes to getting older, micronutrients affect everything, from the molecular level (think telomeres) to the cosmetic (even premature gray hair has been linked to vitamin B5 deficiency as far back as the 1940s).  Micronutrient deficiencies causing disease is not a new idea. It is simply overlooked and often dismissed in the current medical paradigm, which sees aging largely as simply a consequence of time and nothing more. But micronutrients directly affect so many aspects of aging:

  • Micronutrients affect our gene expression.
  • Micronutrients affect how our immune cells work.
  • Micronutrients affect our hormone levels.
  • Micronutrients affect mood and neurotransmitters.
  • Micronutrients affect the repairability in connective tissue (joints, bones, wrinkles)  
  • Micronutrients affect the ability to build and maintain muscle mass.
  • Micronutrients affect our heart and vascular health.
  • Micronutrients affect whether we are more likely to get certain cancers.

In short, MICRONUTRIENTS AFFECT HOW WE AGE.  Nourish the cell, nourish the person.

Here is the good news: You can find out what micronutrient deficiencies you have and correct them. SpectraCell Laboratories has been measuring micronutrient deficiencies for thirty years.  Armed with the knowledge of your personal deficiencies, you can then develop a plan, via supplements or food, or other changes, to correct them and reap the rewards of healthy cell function.  

And here’s the kicker – since the SpectraCell test is performed on lymphocytes (white blood cells), you will also find out how adaptable and healthy your immune cells function. Called the Immunidex, it is the first step in every SpectraCell test.  By first measuring and then correcting (1) micronutrient deficiencies and (2) immune cell dysfunction, you are taking a giant step toward maintaining health and vitality regardless of your chronological age.

SpectraCell has been measuring micronutrient status for 30 years with its Micronutrient Test. Additionally, SpectraCell was the first to commercialize Telomere testing. Aging is more than wrinkles and mindset. Discover how SpectraCell's cutting edge diagnostics in telomeres and cell health are changing the game.

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1Ames B. Low Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage.  Proc Natl Acad Sci USA 2006;103:17589-17594.
2Ames B et al. Mineral and vitamin deficiencies can accelerate the mitochondrial decay of aging. Mol Aspects Med 2005;26:363-378.
3Pantothenic acid, the adrenal cortex, and gray hair.  Nutr Rev 1946;4:84-85.
4Sadighi A. Aging and the immune system: An overview. J Immunol Methods 2018;462:21-26.
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