You will need this so ask your doctor if they are comfortable in testing for this and plugging those 36 holes. A blank stare or non answer, fire that incompetent doctor.
Your chances of getting dementia. Has your doctor warned you about this?
2. Then this study came out and seems to have a range from 17-66%. December 2013.
The following is abbreviated, read the book and demand your doctor read the book.
The first step is what Dr. Bredesen calls a cognoscopy. That involves
blood work, genetic tests and more to identify where the patient stands
when it comes to Alzheimer's 36 causes.
Just like a roof with 36 holes can only work if all 36 are repaired, Dr.
Bredesen says there are 36 causes of Alzheimer's that must all be
addressed. His treatment centers on figuring out exactly why a person is
experiencing cognitive decline and correcting those deficiencies.
| 35 Mechanisms |
| 1. Decrease Aβ production |
| 2. Increase Aβ degradation |
| 3. Decrease Aβ oligomerization |
| 4. Increase BDNF (Brain Derived Nerve Factor) |
| 5. Increase NGF (Nerve Growth Factor) |
| 6. Increase G-CSF |
| 7. Increase ADNP |
| 8. Decrease p-tau |
| 9. Decrease homocysteine |
| 10. Build synapses |
| 11. Decrease 4/2 |
| 12. Increase Aβ breakdown |
| 13. Increase A/G Ratio (Albumin/Globulin) |
| 14. Decrease Inflammation |
| 15. Inhibit NF-kB |
| 16. Increase GSH (glutathione) |
| 17. Increase antioxidants |
| 18. Decrease Iron (& decrease copper, increase zinc – target of Zn : fCu is 100:10-15) |
| 19. Increase CBF |
| 20. Increase ACh |
| 21. Increase α 7 signaling |
| 22. Increase Aβ transport |
| 23. Increase Aβ clearance |
| 24. Decrease ApoE4 effect |
| 25. Increase GABA |
| 26. Decrease NMDA |
| 27. Optimise hormones |
| 28. Increase vitamin D |
| 29. Decrease pro-NGF |
| 30. Decrease caspase-6 |
| 31. Decrease N-APP |
| 32. Increase Memory |
| 33. Increase Energy |
| 34. Increase Mitochondrial function |
| 35. Increase Mitochondrial protection |
| The six principles of the programme developed by Dr Bredesen are as follows: |
| 1. The goal is not simply to normalise metabolic parameters, but rather to optimise them. |
| 2. Based on the hypothesis that AD results from an
imbalance in an extensive plasticity network, the therapy should address
as many of the network components as possible, with the idea that a
combination may create an effect that is more than the sum of the
effects of multiple monotherapeutics. |
| 3. Just as for other chronic illnesses such as
osteoporosis, cancer, and cardiovascular disease, the underlying network
features a threshold effect, such that, once enough of the network
components have been impacted, the pathogenetic process would be halted
or reversed. Therefore, even though it is not expected that most
patients will be able to follow every single step of the protocol, as
long as enough steps are followed to exceed the threshold that should be
sufficient. |
| 4. The approach is personalised, based on the
contributory laboratory values affecting the plasticity network; and is
computationally intensive, since many physiological data points are
analyzed, interdependent network-component status is assessed, and many
interventions are prioritised to determine the therapeutic program. |
| 5. The program is iterative, so that there is continued optimisation over time. |
| 6. For each network component, the goal is to address it in as physiological a way, and as far upstream, as possible. |
A Therapeutic System was developed by Dr Bredesen, referred to as Therapeutic System 1.0.
| Therapeutic System 1.0 |
| 1. Optimise diet: minimise simple CHO, minimise
inflammation – patients are given a choice of several low glycaemic, low
inflammatory, low grain diets. This aims to minimise insulin &
inflammation. |
| 2. Enhance autophagy, ketogenesis by fasting for 12
hours each night, including 3 hours prior to bedtime. This aims to
reduce insulin & Aβ levels. |
| 3. Reduce stress – with a personalised programme of yoga
or meditation or music, etc. This aims to reduce cortisol, reduce CRF,
support the stress axis. |
| 4. Optimise sleep – 8 hours a night, with 1-3 mg of melatonin at night, tryptophan 500 mg 3X per week, exclude sleep apnoea. |
| 5. Take exercise – 30-60 minutes per day, 4-6 days/wk |
| 6. Engage in brain training & stimulation |
| 7. Optimise Homocysteine, < 7, with Me-B12
(Methylcobalamin), MTHF (methylenetetrahydrofolate), P5P
(pyridoxal-5-phosphate), TMG (trimethylglycine) if necessary. |
| 8. Serum B12 > 500, with Me-B12 (Methylcobalamin). |
| 9. hs-CRP < 1, A/G > 1.5 with anti-inflammatory diet; curcumin; DHA/EPA; optimise hygiene. |
| 10. Optimise insulin < 7 fasting, HbA1C < 5.5 – diet as above – with aim to minimise inflammation in AD. |
| 11. Optimise hormones: Free T3, Free T4, TSH, Pregnenolone, Progesterone, Oestradiol, Testosterone, Cortisol & DHEA |
| 12. GI Health – with probiotics and prebiotics if necessary |
| 13. Reduce Aβ levels – Curcumin, Ashwaganda |
| 14. Cognitive enhancement – Bacopa monniera, magnesium threonate |
| 15. Vitamin D3 – 25OH-D3 = 50-100ng/ml – optimise levels with vitamin D3, & vitamin K2. |
| 16. Increase Nerve Growth Factor (NGF) – H. erinaceus or acetyl-l-carnitine |
| 17. Provide structural synaptic components: DHA, citicoline |
| 18. Optimise Antioxidants: Mixed tocopherols & tocotrienols, Se, blueberries, NAC, ascorbate, α-lipoic acid. |
| 19. Optimise Zn: fCu ratio – depends on values obtained |
| 20. Ensure nocturnal oxygenation – Exclude or treat sleep apnoea |
| 21. Optimise Mitochondrial function: CoQ or ubiquinol,
α-lipoic acid, PQQ polyquinoline quinine), NAC, ALCAR
(acetyl-L-carnitine), Se, Zn, resveratrol, ascorbate, thiamine |
| 22. Increase focus – with pantothenic acid for acetylcholine synthesis |
| 23. Increase SirT1 function with resveratrol |
| 24. Exclude heavy metal toxicity – Evaluate heavy metals (Pb, Hg, Cd) – chelate as necessary |
| 25. MCT effects – Coconut oil or Axona |
The rationale behind the desired changes are based on the known role
of inappropriate inflammation in AD and therefore to reduce inflammation
accordingly, & to reduce auto-immune risks, to minimise insulin
resistance, to reduce Aβ, to reduce excess cortisol, to reduce excess
CRF, & support the hypothalamic adrenal axis, to optimise
antioxidant status, to optimise blood glucose balance, to support
optimal production of acetylcholine synthesis.
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