You’re right, we do understand the pathophysiology of many diseases, and those are the ones that have been mostly eradicated. The major chronic diseases that remain are very poorly understood such as type II diabetes, cancer, cardiovascular disease, and alzheimer’s.
I spend a lot of time reading about ‘alternative’ ideas about these diseases, and many seem promising, but aren’t taken seriously by the mainstream. It’s definitely possible that they’re ignored for a good reason, but I haven’t been able to find the reasons yet. This is the biggest problem I’ve found with trying to be ‘critical of everything.’ In very few instances do I find myself quickly understanding and agreeing with the mainstream view. Instead, the more I read the more my opinion seems to diverge from the mainstream view. I have made an effort to discuss these issues personally with specialized experts, so they could help point out factors I may be missing, or not understanding correctly. I am a PhD candidate in the life sciences, so I have the opportunity to meet with research professors at my university in person to help clarify my understanding.
Here are two example theories, regarding cancer and cardiovascular disease in particular.
1) The idea that cancer isn’t initiated by genetic mutations, but that mutations are a downstream phenomena that results after damage to the mitochondria occurs.
This stems from the initial observation by Warburg, that lack of control over glycolysis is part of the cancer cell phenotype. This phenotype can be triggered by a large number of factors which inhibit mitochondrial respiration including hypoxia. Later it was found that the mitochondria in cancer cells undergo a phenotypic change, where the cristae structure is lost. Nuclear transfer experiments have shown that a ‘mutated’ cancer nucleus placed into a healthy cell cytoplasm does not exhibit a heritable cancer phenotype. Conversely, a healthy nucleus placed into a cancerous cell cytoplasm does exhibit a heritable cancer phenotype.
Here is a review article covering the evidence for this hypothesis:
More evidence for this hypothesis includes the observation that active thyroid hormone levels (T3) are inversely correlated with cancer mortality rates in the general population. T3 is a key regulator of mitochondrial respiration:
2) The finding that treatment for hypothyroidism drops cholesterol levels significantly, and virtually abolishes cardiovascular disease without the side effects seen from statins. The late Broda O. Barnes was an experimental endocrinologist and a clinical doctor, and he extensively documented this phenomena in his books and publications.
The idea here is that the central mechanism of cardiovascular disese is a low metabolism which inhibits cholesterol clearance from the blood via reduced steroid hormone synthesis, and reduced bile synthesis. The pathophysiology of cardiovascular disease begins with a long residence time of cholesterol particles in the blood, resulting in their oxidation. This can be reversed by any strategy that restores a normal (higher) metabolic rate: a carefully designed diet and/or thyroid hormone supplementation.
I am not insisting that these ideas are correct, or are some sort of ‘well proven answer’ to these diseases. I’m just pointing out that they seem promising, but are relatively ignored. If they prove accurate, much of the mainstream research on these phenomena would seem to be barking up the wrong tree.
You might notice that both of these examples are essentially the same theory. This is an appealing concept to me: most age-related chronic diseases may be centered around a common process of age related impaired mitochondrial function and/or improper hormonal regulation of mitochondrial function. Insufficient chemical energy (ATP) to fuel normal biological function would have widespread consequences, and could present as a diverse array of seemingly disconnected symptoms. I’ll admit, this sounds somewhat like a modern molecular version of vitalism. However, unlike vitalism it makes specific testable predictions, and involves a very specific mechanism. It’s also consistent with the ‘free radical’ and ‘tissue peroxidizability index’ theories of aging, which involve (among other things) progressive oxidative damage of unsaturated fats (such as cardiolipin) in the mitochondrial inner membrane.
You’re right, we do understand the pathophysiology of many diseases, and those are the ones that have been mostly eradicated. The major chronic diseases that remain are very poorly understood such as type II diabetes, cancer, cardiovascular disease, and alzheimer’s.
I spend a lot of time reading about ‘alternative’ ideas about these diseases, and many seem promising, but aren’t taken seriously by the mainstream. It’s definitely possible that they’re ignored for a good reason, but I haven’t been able to find the reasons yet. This is the biggest problem I’ve found with trying to be ‘critical of everything.’ In very few instances do I find myself quickly understanding and agreeing with the mainstream view. Instead, the more I read the more my opinion seems to diverge from the mainstream view. I have made an effort to discuss these issues personally with specialized experts, so they could help point out factors I may be missing, or not understanding correctly. I am a PhD candidate in the life sciences, so I have the opportunity to meet with research professors at my university in person to help clarify my understanding.
Here are two example theories, regarding cancer and cardiovascular disease in particular.
1) The idea that cancer isn’t initiated by genetic mutations, but that mutations are a downstream phenomena that results after damage to the mitochondria occurs.
This stems from the initial observation by Warburg, that lack of control over glycolysis is part of the cancer cell phenotype. This phenotype can be triggered by a large number of factors which inhibit mitochondrial respiration including hypoxia. Later it was found that the mitochondria in cancer cells undergo a phenotypic change, where the cristae structure is lost. Nuclear transfer experiments have shown that a ‘mutated’ cancer nucleus placed into a healthy cell cytoplasm does not exhibit a heritable cancer phenotype. Conversely, a healthy nucleus placed into a cancerous cell cytoplasm does exhibit a heritable cancer phenotype.
Here is a review article covering the evidence for this hypothesis:
Cancer as a metabolic disease: implications for novel therapeutics http://carcin.oxfordjournals.org/content/35/3/515
More evidence for this hypothesis includes the observation that active thyroid hormone levels (T3) are inversely correlated with cancer mortality rates in the general population. T3 is a key regulator of mitochondrial respiration:
Thyroid hormones and mortality risk in euthyroid individuals: The Kangbuk Samsung Health Study. http://www.ncbi.nlm.nih.gov/pubmed/24708095
2) The finding that treatment for hypothyroidism drops cholesterol levels significantly, and virtually abolishes cardiovascular disease without the side effects seen from statins. The late Broda O. Barnes was an experimental endocrinologist and a clinical doctor, and he extensively documented this phenomena in his books and publications.
The idea here is that the central mechanism of cardiovascular disese is a low metabolism which inhibits cholesterol clearance from the blood via reduced steroid hormone synthesis, and reduced bile synthesis. The pathophysiology of cardiovascular disease begins with a long residence time of cholesterol particles in the blood, resulting in their oxidation. This can be reversed by any strategy that restores a normal (higher) metabolic rate: a carefully designed diet and/or thyroid hormone supplementation.
Here is a good introduction to this idea:
The Central Role of Thyroid Hormone in Governing LDL Receptor Activity and the Risk of Heart Disease http://blog.cholesterol-and-health.com/2011/08/central-role-of-thyroid-hormone-in.html
I am not insisting that these ideas are correct, or are some sort of ‘well proven answer’ to these diseases. I’m just pointing out that they seem promising, but are relatively ignored. If they prove accurate, much of the mainstream research on these phenomena would seem to be barking up the wrong tree.
You might notice that both of these examples are essentially the same theory. This is an appealing concept to me: most age-related chronic diseases may be centered around a common process of age related impaired mitochondrial function and/or improper hormonal regulation of mitochondrial function. Insufficient chemical energy (ATP) to fuel normal biological function would have widespread consequences, and could present as a diverse array of seemingly disconnected symptoms. I’ll admit, this sounds somewhat like a modern molecular version of vitalism. However, unlike vitalism it makes specific testable predictions, and involves a very specific mechanism. It’s also consistent with the ‘free radical’ and ‘tissue peroxidizability index’ theories of aging, which involve (among other things) progressive oxidative damage of unsaturated fats (such as cardiolipin) in the mitochondrial inner membrane.