Lipofuscin: Is Your Brain Ready to Rock… or Rust?
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Lipofuscin is the ‘age related pigment’ that accumulates in certain cell types, notably neurones, kidney, retinal ganglions, liver, heart and adrenals. If you look at the skin of an older person, you might see brown patches, so called ‘liver spots’ (probably called that, now that I think about it, because their colour is close to that of raw liver – dark tan) that become apparent usually during the 6th decade onwards. Lipofuscin is a pigment, byproduct of the oxidisation of unsaturated fatty acids (so you can see how inevitable its accumulation is – we ALL metabolise fatty acids every day). It contains sugars and heavy metals also.
What causes it?
Aside from certain medical conditions, where abnormal levels of lipofuscin accumulate rapidly, lipofuscin buildup within cells is a normal part of ageing and cellular metabolism. Basically, organelles within cells, called lysosomes, whose function is a kind of ‘cellular cleanup crew’, generate lipofuscin as a byproduct of the work they do digesting old bits of cellular machinery. This allows space for new, shiny bits of cellular machinery – vital in a space-restricted setup like the cell.
How does it affect me?
Lipofuscin is sometimes called ‘cellular rust’ and whilst this terminology does a good job of conveying some of the negative effects of lipofuscin (basically ‘aging’ the cell, compromising efficiency, but not actually killing the cell), lets look more closely at the mechanisms associated with lipofuscin accumulation.
Lipofuscin can be seen to accumulate primarily around the nucleus of a cell. Since the nuclear membrane contains many receptors, critical for initiating the generation of new cellular protiens, and since cellular proteins are fundamental to the function and structure of the cell, you might agree with the author that by gathering around the nucleus, lipofuscin has the potential to significantly degrade cellular function. And indeed, it seems to. Not to the point of cellular apoptosis (programmed cell death – a vital part of healthy cellular life), but to the point where we begin to notice compromised function and label it ‘old age’.
Now I am not saying that lipofuscin is entirely responsible for how we lose functional capacity during our twilight years, since there are other factors (e.g. reduced cerebral blood flow, hardening of blood vessels, altered hormone levels), but I posit that since EVERYTHING in the body has some degree of cellular origin, reduced cellular function plays a significant part in the aging process.
What can I do about it?
NOTHING! Hahaha, I’m only jesting with you, dear and esteemed reader, there are things that one can do as part of an intelligent management plan to control and even reduce lipofuscin levels.
Firstly, one might look at reducing the input of those compounds found in lipofuscin, in the hope that the ‘downstrem’ results might be reduced generation of the age pigment. Well, OK, that would be a noble and purist approach, but would require a lifetime of ascetic living and is (in this authors opinion) by no means guaranteed to work. I have seen no studies on this approach.
However I HAVE seen studies (and you, the diligent nootropics researcher should attempt to seek them out on pubmed, just as I have done) that show that:
DHA (an omega 3 fatty acid) prevents age-related A2E (one of the most studied/characterised components of lipofuscin) accumulation within the retina (mouse study).
Prevention of age-related degeneration in neural function and healthy brain ageing can be achieved with long-term use of bacosides (bacopa monnieri) (rat study).
Grape seed proanthocyanidin lowers brain oxidative stress in adult and middle-aged rats.
That vitamin E reduced lipofuscin accumulation by 50% in intact nerve ganglions (snail study).
…And that adding retinol (vitamin A) to your vitamin E will enhance this effect (rat study).
Now many experts agree that one of the important factors in controlling age-related decline in neural function is to control cellular oxidation. They also state that reversal of lipofuscin accumulation should be a ‘gold standard’ in the prevention of neural degeneration diseases like alzheimers, etc.
One compound that has shown a lot of promise in preventing accumulation of lipofuscin (as well as being an all round ‘nice guy when it comes to your brain and body) is vinpocetine. If you are familiar with this author, then you will know that he strongly supports vinpocetine use both as a genuine nootropic and as a ‘neural protectant’, since it has been shown to exert powerful neural anti-oxidant effects. Vinpocetine can be used to directly counter some of the effects associated with senile cerebral hypoperfusion (as we get into old age, the brain often experiences reduced blood vessel number and lumen size, resulting in poor blood supply) by acutely increasing blood supply, O2 utilisation and ATP synthesis within the brain.
Of course, one would have to take vinpocetine (or any other anti-oxidant) for many years, as a prophylactic measure, to have any significant effect on lipofuscin accumulation.
The clever supplement user might also want to supplement with NAC, since this will facilitate synthesis of the bodys primary endogenous anti-oxidant – glutathione.
However if we want to actually remove existing lipofuscin deposits, then we need to look at another compound, namely centrophenoxine. This compound has been shown to accelerate the removal of lipofuscin pigment (LP) and ceroid pigment (CP) accumulations, by decrease and dissolution by cytoplasm rehydration, optimization of the brain cellular recycling system activities, by neuronal, glial and capillary LP lysis and CP lysis, by neurono-glio-endothelial transfer of highly processed LP and CP, with final capillary elimination.
How do I create an optimal strategy for lipofuscin removal and management?
We would suggest that the nootraveller begin with a short period of intense Centrophenoxine use. 3 weeks @ 2000-4000mg/day should be enough to effect some worthwhile lipofuscin removal. We then need to inhibit buildup of LP with vinpocetine and other neural (and non-neural) antioxidants, such as grapeseed extract, acai, etc.
But since exogenous anti-oxidant use may down-regulate the endogenous network, we recommend alternating periods of anti-ox use with periods of NAC use, to facilitate optimum function of the endogenous network. The ideal anti-oxidant solution? Neuroprime, which is formulated following these guidelines.