We all do need to find some ways to balance out our health.
As a biochemical engineer by trade, we do learn early on that it is desirable to operate complex process units on the basis of a steady state for easier control and management.
The definition of a steady state is "an unchanging condition, system or physical process that remains the same even after transformation or change". It is a form of a dynamic equilibrium, where things can enter and exit a system without changing the state of the system.
There is a balance involved. In terms of mass: if I am feeding X kilograms of material into a unit each hour, I should expect to get X kilograms of material out each hour. If I were to get less than X kilograms of material per hour out of the unit, then where is the remaining material?
Is it accumulating within the unit? Is it stuck somewhere? That would have a significant impact on my design and my operations.
However, why is it the case that a lot of people don't understand the reason why they put on weight is because... they're putting more mass into their bodies than their bodies are eliminating? (It may be a simplistic analysis here, but a lot of people do put on weight because their calorie input is much higher than their calorie output - which did happen to me, I was formerly more obese than I am now).
Our bodies are operating at a steady state
Part of the weight management is to eat less and to exercise more, which does indicate that our energy input and output has to be balanced out in a steady state. Most medically healthy people are able to lose weight by controlling their calorie intake and by exercising more.
But what other steady state mechanisms are there that we may not necessarily be aware about?
Let's look at our bones, for instance.
The bone structure of a teenager at puberty is not at steady state. There is room for a growth spurt. One doesn't experience a height increase if their leg bones remain the same length throughout.
However, upon reaching adulthood, our bones reach a dynamic equilibrium. It's not a static equilibrium. It is said that "static equilibrium occurs when there is no exchange between reactants and products."
But our bones comprise numerous live cells, and that complicates the analysis. The bones do not comprise non-living calcium mineral. There is more than meets the eye.
There are 3 major types of bone cells, the osteoblasts, osteocytes and osteoclasts, which can be described as such:
OSTEOCLASTS are large cells that dissolve the bone. They come from the bone marrow and are related to white blood cells. They are formed from two or more cells that fuse together, so the osteoclasts usually have more than one nucleus. They are found on the surface of the bone mineral next to the dissolving bone.
OSTEOBLASTS are the cells that form new bone. They also come from the bone marrow and are related to structural cells. They have only one nucleus. Osteoblasts work in teams to build bone. They produce new bone called “osteoid” which is made of bone collagen and other protein. Then they control calcium and mineral deposition. They are found on the surface of the new bone.
When the team of osteoblasts has finished filling in a cavity, the cells become flat and look like pancakes. They line the surface of the bone. These old osteoblasts are also called LINING CELLS. They regulate passage of calcium into and out of the bone, and they respond to hormones by making special proteins that activate the osteoclasts.
OSTEOCYTES are cells inside the bone. They also come from osteoblasts. Some of the osteoblasts turn into osteocytes while the new bone is being formed, and the osteocytes then get surrounded by new bone. They are not isolated, however, because they send out long branches that connect to the other osteocytes. These cells can sense pressures or cracks in the bone and help to direct where osteoclasts will dissolve the bone.
Our bones, therefore, maintain a dynamic equilibrium when the rate of bone formation (via osteoblast activity) equals the rate of bone dissolution (via osteoclast activity). This dynamic equilibrium allows damaged bone segments to be eliminated by the osteoclasts, so that osteoblasts can synthesise fresh bone mineral to fill in the damages. Hence, the structural activity of the bone can be preserved.
However, with the body being a complex mix of biochemical reactions and signallers, this dynamic equilibrium can be easily disrupted. For example, when one is obese, their excess fat cells will be signalling their immune system's macrophages to produce more interleukin 1-beta (IL-1β). IL-1β is a pro-inflammatory cytokine that is a significant player in various situations, including promoting osteoclast activity (while not influencing osteoblast activity at all).
And when an increased osteoclast activity causes the rate of bone dissolution to increase, while osteoblast activity remains roughly the same (or the rate of bone formation remains constant), then would the person not be at a higher risk of a weakened bone structure over time (osteopenia or osteoporosis)?
Is it any surprise, then, that obesity has been classified as a risk factor for osteoporosis?
Let's have a look at our joints as well.
Again, in the spirit of dynamic equilibrium, we have two different cell types: the chondrocytes and the synovial cells. The chondrocytes are responsible for producing the collagen matrix that comprises our joint cartilage, while the synovial cells are responsible for the elimination of any damaged cartilage.
The synovial cells eliminate damaged cartilage by producing matrix metalloproteinase (MMP) enzymes that will digest the collagen matrix, such that the chondrocytes can produce fresh collagen to replace the damaged cartilage. Hence, when we do suffer a joint injury, it is wise for us to rest that joint and allow the MMPs to remove the damaged cartilage, as well as to allow the chondrocytes to produce fresh cartilage replacements. All that takes time.
Because when we do suffer injuries or irritation to our joints, the synovial cells are signalled to produce more MMPs by the pro-inflammatory cytokine IL-1β (again!). If we do not allow the injury to heal properly, but continue working or exercising the injured limb, there will be that constant pro-inflammatory IL-1β signal lingering there.
When the IL-1β signal lingers, MMP activity remains higher than normal and continues digesting joint cartilage.
Hence, insufficient rest and recovery for an injured limb can potentially lead into a situation of osteoarthritis. Isn't that the case for highly active sports players who do not rest their injuries sufficiently? They are at higher risk of developing joint problems as they age.
And could that be another reason why, then, that obesity can be a risk factor for osteoarthritis too?
It's a dynamic equilibrium that we're looking at.
And it's definitely biochemical in nature - the cellular activity that is involved in bone/joint formation/degradation.
When we're looking at calcium supplementation as a safeguard against osteoporosis or glucosamine supplementation as a safeguard against osteoarthritis, the main question that we have to be asking ourselves is:
How do these supplements even influence the dynamic equilibrium in our body?
We'd find that calcium alone wouldn't be useful for protection against osteoporosis, while glucosamine alone wouldn't be useful for protection against osteoarthritis.
In fact, for bone health, there would be at least 9 Nutrients To Support Healthy Bone Development, while there are at least 10 Nutrients That Support A Healthy Joint Function.
But firstly, we do need to understand the bone/joint formation/degradation processes at the cellular level. It's something that the doctors don't really talk about, do they?
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This article was originally published on Vocal.
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