Why are some people more prone to addictions than others? Why do some crave the "hit of the high", where others can enjoy a substance or an experience and leave it behind?
Most of us think of addiction pertaining to illicit or mind-altering drugs, but what about peoples' addiction to alcohol, religion, sugar or even exercise?
In today's podcast, we welcome back Elizma Lambert, Naturopathic specialist in complex cases, to take us through the important factors to consider with addiction. From uncovering why our brain's reward centre is being hijacked and our excitatory system being supercharged, to individualised patient support strategies. Listen to Elizma show us how to connect the dots so we too, can better support our patients with addiction issues.
Covered in this episode:
[00:44] Welcoming back Elizma Lambert
[01:51] Is addiction in our genes?
[02:49] The DRD2 A1 gene
[04:16] Nature vs. Nurture?
[07:22] Genes: The roadmap of risks
[10:13] Addiction to exercise
[13:54] When are these patients presenting in practice?
[15:03] How can we measure or assess?
[19:27] The delicate balance of dopamine
[23:54] Addiction to stress
[27:29] Prescribing GABA
[32:31] Don't just give a band-aid solution
[35:30] Figuring out the drivers of inflammation
[37:35] Medical co-management
[39:10] Where to access further resources
Andrew: This is FX Medicine, I'm Andrew Whitfield-Cook. Joining me on the line today is Elizma Lambert. Who's both a qualified naturopath and homeopath with close to 15 years experience who runs a busy practice and is involved in practitioner education. She always takes a generalist approach in the way she teaches and treats her clients, as she believes that there are too many specialists and not enough practitioners who see the big picture.
Applying her knowledge on cellular biochemistry and genetics enables Elizma to navigate treatments for many different diseases and disorders. She's becoming well known for her ability to connect the dots between root cause, symptoms, and genetics. And helping people to reach a better understanding of their health conditions.
She travels regularly to Europe and the US to learn the latest techniques and connect with well-known and respected practitioners, but her clients are her true teachers. You can learn more about Elizma at mthfrandbeyond.com.au.
Welcomed with FX Medicine, Elizma, how are you?
Elizma: Very good. Thank you, Andrew.
Andrew: Now, we're going to be talking about a very controversial subject and one which needs more attention in our community. That's the genetic predilection to addiction. So, I guess we need to start off with what are we really talking about with regards to the genetic predilection?
Elizma: Okay, well, if you look at the definition of addiction, it's a compulsive engagement in a behaviour that is naturally rewarding despite the adverse or the negative consequences that follows it.
But there was a lot of research that was done by Dr Kenneth Blum, who is doing a lot of research in neurogenetics and neurogenomics. And based on the research that he has done, the definition of addictions have somewhat changed, highlighting that addiction is more of a chronic brain disorder and not simply a behavioural problem of too much indulgence.
So, I guess what I'm trying to say is that addiction is not a psychological disorder but more of a physiological disorder. And this is because there's a lot of neurobiochemistry that gets disrupted with addictions and they are also now finding a lot of genetic components that can make a lot of people more prone to addictions. Or put them at higher risk of developing addictive behaviours later on in life. And one of the major genes involved here is the DRD2 A1 gene.
Andrew: Is this the reward-seeking?
Elizma: Yeah. That's correct. That's the gene involved in the reward deficiency syndrome. Or RDS as it's sometimes called.
So, that one's probably received the most attention. There's a lot of other genes that will be explored as well. The dopamine transporter DAT1. It's another gene that plays a huge role here. And my understanding is that Dr Blum is working on a panel of about 10 genes, or 10 polymorphisms, to sort of create a risk factor score, for people who might be at high risk for developing addiction. So that these people can be screened early on and it may sort of like, change the treatment of a lot of these people by looking at the genetic variants.
Andrew: But with regards to that gene. Surely, there's environmental factors that cement the behaviour, is that right?
Elizma: Absolutely. The gene pretty much gives you about a 74.4% increased risk of developing addictions. But the environmental or epigenetic factors has a role of, you know, I don't really know how to find these percentages, but according to the research, it can reduce the risk of that gene expressing by 30% to 50%. So, your genes is not your destiny. There's absolutely a lot of environmental factors that can determine whether you're going to express those genes or not.
I guess the problem in all of this is you don't necessarily have to be ever exposed to alcohol or drugs to develop an addiction because an addiction can come from just from ordinary diet. Just from the sugar in our diet. Or from… you can become addicted to exercise. So, there's a lot of other things that you can become addicted to that doesn't necessarily get recognised as a problem because it's not a drug or an alcohol. And no one ever really sees it as a problem and it may not necessarily be a problem, but you can still have those addictive traits when you have these genetic risk factors. But it might not necessarily translate to an alcohol or drug addiction.
Andrew: You know, that's a really interesting comment you make. Because a very wise practitioner, who was a colleague many years ago, we were talking about, I think it was prisoners, criminals who had found religion in prison. This wise practitioner said they're just swapping one addiction for another. And they become so fixated then on the religion as their outlet if you like of their addictive behaviour.
Elizma: Yeah. That's absolutely true. Yeah. Because it all follows the same...it's still a dysregulation in the dopaminergic reward system. So, there's been many substances and many behaviours that can feed into this system. And so if you take one away, then people are inclined to just substitute with another one.
You know, it's the same with smoking. How many smokers start to overeat? How many alcoholics start to overeat when they start giving up alcohol? So, you are just really swapping one for another. And it's interesting that she was mentioning about the prison system. Because if you look at the DAT1 or the dopamine transporter, if that comes into play with a DRD2 and it really amplifies addictive behaviour, that one specifically is very much associated with violent behaviour as well.
So, it would be interesting if you ever could do the genetics of a lot of prisoners, you know, who are in there for are violent alcoholic outbursts or crimes that involve drugs. It would be really interesting to see what the genetics look like. Because if you just have the DRD2 genes, you might not necessarily have those violent tendencies, it's just an addiction. But I thought it was quite interesting.
Andrew: And this is the thing that gets me about how medicine is sort of...I get the caution of medicine with regards to genetics, but I don't get the dismissal by some quarters of the medical profession of genetics. Of SNPs and things like that. Because boy, I just see in times to come that this is going to give a roadmap of risk. And we're quite happy to look at risk factors for Alzheimer's. We're quite happy to look at risk factors for cardiovascular disease. Why are we not? Why are we dismissing still? Or there's real reticence to accept that our genes are with us. They're here. They're not like something that you might run into. You have them. And I get that they're not a given that you're going to get a disease in the future, but boy, it gives you a roadmap of risk.
Elizma: Oh. Absolutely. If you just look at the risk factor of the DRD2 I mean, that's a case in point. That was such a huge, huge, huge correlation.
One of the most interesting things is that I actually found that in families where this reward deficiency syndrome is really strongly expressed, they found that the man and a woman in a marriage relationship, they both have the gene. So, this seems to be this attraction between people with addictions, which I thought was fascinating. It's literally like the DRD2 genes call to each other.
So, they find this really high correlation with men and women with DRD2 genes getting married. And this is not just in families with really, really strong expression. I'm not suggesting that everyone with addictions do that.
But there is a strong predilection and if we ignore genetics, I mean this is, in my opinion, one of the reasons why so many of the drug treatments fail. Because the relapse rate is just enormous. And I think this is because we are ignoring the dopamine receptor expression and a lot of the genes involved in that. And if we can screen people, and I think we need to also be very careful with that because there's a lot of fear of being boxed into an area or having their insurance denied because they've got some kind of a genetic predisposition.
So, I think there's still a lot of things that needs to be sorted out there. But if we could use it for good and we could use it to screen people and in so, change our lifestyles and our behaviours and be aware of where we need to be careful of, then it could just prevent so much problems down the line, you know?
Andrew: Something that you said earlier, I'm just checking myself on and that's with regards to this… an addiction to exercise or an addiction to religion. You said something about that you keep doing it despite having negative consequences. So, therefore, we know that excessive intake of sugar leads to metabolic disease, diabetes, cardiovascular disease, stroke. We know that smoking tobacco, drinking alcohol, taking illicit drugs, certain illicit drugs, have adverse effects on not just self but family community, we get that. But what about exercise?
Elizma: Well, as someone who used to be addicted to exercise myself, I can say that anything is good in moderation. But even something as good as exercise can have negative consequences. Because what can happen is your body doesn't get the recovery time that it needs. So, you can ignore all of those signals that your body is telling you that you need to take it slow, that you need to maybe change your exercise, have more recovery days. You ignore those things and your push through and you develop injuries, chronic muscle breakdown, chronic tissue breakdown and end up with injuries. Then you can't exercise. So, then you're plunged into a huge depression because now you're not getting your dopamine high. You know, and that can put you at risk of then grabbing onto other things to get that dopamine high.
So, this is the spiral that a lot of elite athletes… I mean, we've seen it with Grant Hackett. A lot of these elite athletes can run into this problem when they can't exercise anymore because their bodies have just broken down. They will grab onto something else to get the same kind of feeling. So, yeah. Even exercise in excess can have negative consequences.
Andrew: You spoke about a personal journey with an exercise addiction. How would a practitioner, if you went to see them, tease an addiction to exercise apart from an eating disorder?
Elizma: Yes. Well, for me, if I would usually have a huge questionnaire and based on the questionnaire, I can figure out what's going on in their biochemistry to a large degree. I guess this is where you have to ask them other questions.
When it becomes...when exercise becomes disruptive to the social interaction with other people, when it becomes an obsession. I can remember a time when it was Christmas Day. The gyms will be closed on Christmas day and I would be like, "Well, what do you mean the gym is closed on Christmas Day? So it's that really absurd kind of, addiction. Everything just revolves around that.
Andrew: It's like an OCD thing. Isn't it?
Elizma: Yeah. It's an OCD. Everything revolves around that. If they can't exercise that day, they are miserable. And so that's when things become really pathological. But this is where careful questioning from the practitioner's side needs to be engaged in. You can often also just look at the person and see you know, oh is their body being broken down. In like a catabolic state. Are they obviously taking things too far? Is that all they can talk about?
So, I guess when everything becomes fixated around something, then that is an addiction.
Elizma: But that will require a careful observation and careful questioning of a practitioner and reading between the lines. See if they might have had past addictions. Maybe they used to be obese and now they are gym junkies. So, they've substituted carbs and sugar for exercise. It's looking for patterns in their lifestyle.
Andrew: When do you see this sort of patient in your practice? Do you see them at the beginning or when everything else has failed?
Elizma: Well, I've seen them generally when everything else has failed. Because a lot of people would have tried hypnotherapy. A lot of them would have just tried going cold turkey. Whether it's to do with the food addictions or nicotine addictions or alcohol addictions or drug addictions.
And so it's usually when they've realised their willpower is just not winning out on this battle for them. And when all other therapies have failed. That's when we start looking at biochemical reasons. Because I feel that that is often being missed. Because we see addictions largely still, as a psychological disorder. So, we'll put people in therapy or put them on programs. We are often still missing the biochemical aspects here, which has got more to do with neurotransmitter dysregulation and receptor resistance. So, that's usually I would see them at those later stages when everything else has failed.
Andrew: You know, I'm still wondering in my mind about it was a slideshow that I saw and I'll put this up on the FX Medicine website for our listeners and that was by John Saunders at Sydney Uni, Southwest or South Pacific private. And it was titled "Understanding Addictions Perspectives from DSM5 and ICD11." It was a presentation that he gave.
And gee, there was some good information on there. One of the interesting things that I remember reading was about the how the reward system became underactive because it's been hijacked by the addictive process. Then the excitatory system is hyperactivated in response to whatever substance you're addicted to. Can you measure this? And if so, how do you measure, or to decide that it is actually an addictive process going on?
Elizma: That's a really, really good point. I would love to see the slides that you're talking about, Andrew. That sounds really interesting.
He's certainly correct. Like what happens is you have this underactive dopaminergic system and so you're trying to drive up the dopamine to get the high. But the problem is, is when this happens in a chronic situation. Especially if the receptors, the dopamine receptors are down-regulated. It's the same as insulin resistance. You have to produce more and more and more dopamine to get the high.
Now, because you're producing so much dopamine, you are now shifting the bar, so to speak. Because we all will have a level. Let's say if we take the normal level of dopamine, and once we get there, we feel great. Everything's fantastic. Now, if you keep on having to produce more dopamine because the receptors are not sensitive enough, then you're going to raise that bar. So, now a normal level of dopamine is not enough for you anymore. You always have to go for that higher level. And so that's why even at normal dopamine levels the body will still be in a low dopaminergic state for that person. Because the messages are just not getting through.
Now, how you measure that, that's a very interesting idea, and I guess at this point in time, the best way that we can measure it, is by doing something like let's say, a urinary neurotransmitter test.
Elizma: Which is the base thing that we've got to measure neurotransmitters because we can't measure, CSF neurotransmitters. So, you can do like a urinary neurotransmitter test. And then you could possibly do something like an organic acid test for instance, which is another urine test. And that way you can measure the actual dopamine in the system and then you can measure the dopamine breakdown products in the system.
And I guess from that you can sort of start putting some of the puzzle pieces together and how much dopamine is being produced? How much dopamine is being broken down?
Because if you have to produce a tonne of dopamine to get a message through and the body's not really using that dopamine, so, it has to do something with it. It'll tend to… it will have to put it through the COMT enzyme to break it down and through MAO to break it down. So, you can look at those byproducts and you can look at the dopamine production and possibly, that can give you a lot of clues of what may be going on in this person's system.
The trick in here lies with that, it will change depending on the stage there are in. You know, in the beginning, the dopamine levels may be actually quite high. Whereas towards the chronic stages of addiction, you know, after years and years and years, it may be really low because it's like it's depleted.
Elizma: You know, there's not that much left anymore. So, you have to take everything into context. It's not a set standard markers or levels that you could look at. You have to put into context with how long has this been going on? And there may be other genetic variabilities apart from the DRD2. Like COMT and MAO gene mutations as well.
But those can start to form a picture in your mind about what could be going on with this person. But then you can also check...you know, there's also a role with dopamine and insulin, and dopamine and thyroid hormones. So, I think it's getting a really complete picture that's going to give you the better answers at the end of the day. So, a lot of investigative work.
Andrew: With regarding dopamine, and you spoke about the acute versus the chronic phase. In my head, I'm just wondering if there might be some link or hint with regards to, let's say, particularly females, in the beginning stage that they tend to not suffer from cyclical mastalgia with regard to their periods. Because they've got a lot of dopamine, which is as we know, prolactin inhibiting hormone. That's the other name for dopamine. Versus the chronic stage where they end up with worse breast pain because their dopamine is depleted. So, therefore, they've got nothing to antagonise that prolactin. Do you ever see that?
Elizma: Yeah. Absolutely. That is absolutely happening. I think low dopamine is a bigger issue in women than what we recognise.
I mean, dopamine will, first of all, it will naturally tend to drop off after menopause as estrogen levels drop off anyway. So, that seems to be a thing that happens and why a lot of women when they go into menopause become more depressed etcetera.
But when they are not going through menopause and they still have some active hormone production, and that dopamine gets depleted because of just stressors really pushing that system, then yeah. Absolutely. You can start seeing a change happen. And I have seen that where women's PMS symptoms change. They'll say, "I used to have lots of breast tenderness, but now that doesn't seem to be an issue anymore. My issue now is that I have no libido." And that low libido would be more associated with the depleted dopamine.
So, yeah, there’s a huge interplay between the neurotransmitters and hormones and they don't occur in isolation and they don't work in isolation. So, yes, you can see this changing pattern.
Andrew: Another idea that's coming to mind is, from a very kind practitioner who showed me her biofeedback machine. And I'm just wondering about if you could use something like that to assess whether somebody is in this hyperactive state.
And I guess I should explain this. It was a visual computer-generated image where you had a peaceful scene. And depending on if your sympathetic nervous system was activated, was depending on what would happen in that scene that was projected on the computer. It was very weird. Though, I remember being so skeptical at the beginning and then I changed it and I was like, "This is really quite strange." It was really fun to do. And I thought, what a great way to initiate this feedback where the patient can really… not just control, but measure how they're affecting change in the nervous system.
Elizma: I think I saw it in many, many years ago when they were measuring beta waves and alpha waves and things like that in the brain. And yeah. So, didn't see with the pictures, but that's really, really cool if they've changed the program to do that.
And absolutely, because the dopaminergic system becomes over-activated when the body’s more in a sympathetic state. So, the reason why it becomes over activated is because you're losing a lot of those inhibitory neurotransmitters like GABA and serotonin because of no depletion along the line or for various other reasons.
So, if you can control your parasympathetic sympathetic nervous system, and control your stress level, so to speak, you can absolutely start to affect these neurotransmitters and hormones. And that's through, you know, behavioural therapy.
Ultimately, I think that is an amazingly good tool and probably more of a permanent resolution to fix a lot of these issues. Because you're changing behaviour or you're teaching yourself to behave differently in certain situations.
Because I think that's one of the big things we have this stressful society and you get into these patterns and you just can't get out of the pattern. And so we become essentially addicted to stress, in a large way.
Andrew: Yes, yes.
Elizma: So, we have this constant dopamine high. So, even your executive comes back from work, he can't sit and relax because he needs that dopamine rush. So, he'll have alcohol or something like that. So, he's always trying to keep that over-excitation happening. Which works for a certain period of time, but then everything else gets depleted. So, if you can modulate behaviour like that, you know, that's a very, very powerful tool.
Andrew: Now, that's an interesting thing you said, “Addicted to stress.” I think a 21st-century lifestyle. It's like “Welcome to it.”
But, okay. So, let's talk about being addicted to stress. That you know, "I function under pressure" which obviously is deleterious when it's chronic. We're going to run ourselves into the ground. That's what we call overstressed.
How, therefore, when one is in that pit, when one is right there at the point of the craving, and whether this be food, alcohol, illicit drugs, sugar, whatever that be. How can you change, or how can you make patients aware that it's happening right now and you need to activate something. Rather than just going, "Oh, I'll just do it again."
Elizma: You know, I guess from a monitoring perspective because people when they're in the state, they don't realise that's the way they are behaving. You don't recognise these patterns when you're in that state. You just want the fix.
So, I guess if you wanted to monitor it, you know there’s… and I’m not a very savvy with these things, but you can get heart rate variability monitors. There’s so many apps and gadgets and things out there.
Elizma: Some of them really, really easy, you know, like clips on the ear or clips on a finger that can monitor sympathetic and parasympathetic response.
Andrew: Ahh yes.
Elizma: And I've had quite a few clients who use that and that it has changed their behaviour. Because they are stress addicts. They never sleep. They just work, work, work, work, work. And they train, train, train, train, train. And then when they started using these devices, it's like, the thing let's say beeps or whatever. But it alerts you when you need rest. And they start to like, "Oh. Okay. I need to slow down." And I have found that remarkably, a lot of them have just calmed down so much. They've changed their behavior because they get alerted to it in real time.
So, that way, it's not like you have to go to the practitioner to get the test done. It's just a matter of keeping monitoring yourself during the day and then getting these alerts when you are going into that state. That'll be a good way to sort of monitor it.
But then there's also, you know, if you wanted to treat it from a biochemical perspective, there's a lot of nutrients and herbs and things you can use as well. To help and modulate this dopaminergic function and correct things over time too.
Andrew: Just before we move on to nutrients and herbs, which I think obviously is what we need in practice. But you said something there regarding a clip for the ear. And I've spoken to Emrys Goldsworthy about vagal nerve stimulation. With the, forgive me if I get this wrong, Emrys. It's a clip that goes on the internal concha of the ear? So, it's not just a treatment but a monitor.
Elizma: Yeah. As far as I’m aware, there's a monitor. Yeah. It takes data. It draws little graphs. You can track, you can exactly see when those stressful periods are and when you're relaxing. You can track your sleeping patterns, your exercise patterns.
And this is… people who love data collection, they'll love this kind of stuff. Because they can really… even with food, for instance, there's a lot of food that can trigger an adrenaline response as well. Food allergies, food intolerances will trigger this excitation response. So, you can even sometimes time it to meals and then say, "Well, what am I eating in that meal that is driving my sympathetic nervous system?"
So, there's a lot of really cool information that you can get from these kinds of devices.
Andrew: So, with regards to nutrients and herbs and I've got a couple of ones that are just dear to my heart. The first one is the, if you're like, the poster child of relaxation, the mineral, and that would be magnesium. And the herb, of course, for anxiety would be kava.
How often do you use these? And do you check the patient and align the choice of therapy with the patient? Or do you tend to sort of say, "Yep. This work for most patients so I use them all the time?
Elizma: I have my favorites. I'll be honest. I think we all have those traps where we have our favorite things that we always go to first. I certainly do kava, magnesium, great. Because they, especially kava, works on the GABAnergic system which quiets down that dopamine, that stress response.
So, I like to use GABA quite a bit which could work similarly to kava. There’s other herbs, if you want to tone more on the dopaminergic system, you can use herbs like Rhodiola. Which is a very prominent dopamine herb because it enhances the release of dopamine synapse that can then combine with the post-dopamine D2 receptor. And to a large degree, it also inhibits the MAO-A enzyme activity which then can allow for more residual dopamine to be transferred to the vesicles of pre-synaptic neurons for higher dopamine release. So, that can sometimes quieten down a lot of cravings.
So, it gives them that dopamine fix and then they don't need to do anything else to get their dopamine levels up. So, that's really another nice herb to use. And then you know, you've got your N-acetyl cysteine which is another one that can also drive the glutamatergic systems to release dopamine at the nucleus accumbens, which is where the reward site of the brain is situated.
Elizma: Yeah! So, I'll adapt therapies depending on some of the other symptom features as well. So, I can find things that will sort of cover a wide range of things. So, there's quite a few amino acids and herbs that you can play around with when it comes to the dopaminergic system.
Andrew: Now, I've read a lot, there's a bit of controversy where the GABA actually crosses the blood-brain barrier when you give it orally. However, there's other work that shows that, okay, that might be the case, but let's talk about the gut-brain axis. How do you think it's working?
Elizma: Yeah. No. I agree. Like from my research, it won't cross the blood-brain barrier in its intact state unless the blood-brain barrier has been damaged or compromised in some way.
Andrew: Oh, of course, yeah.
Elizma: So sometimes if someone gets a really good result from oral GABA it could be another maybe telltale sign that they might have a compromised blood-brain barrier.
But you are correct. Like I think a lot of the GABAnergic activity can come from the gut itself. Because there are GABA receptors in the gut. So, that might be why a lot of these powders and capsules work.
You can use other forms of GABA that are supposedly crossing the blood-brain barrier as well. I don't think they’re really available here in Australia. But there's your PheniTropic GABA, I think is one that crosses the blood-brain barrier?
But you know, you don't always have to get things into the brain. It's exactly like you said, there's this connection between the brain and the gut. So, you can work on GABA from a gut perspective, but you can also work on it from a hormonal perspective. Because there's a huge relationship between progesterone and GABA as well. So, you lift the progesterone up and go to a low in progesterone and that could also have a GABAnergic effect.
So, that's why you have to look at the whole person and decide, "Well, should I be treating this from a hormonal perspective or a gut perspective or you know, whichever perspective." And now they'll have a flow-on effect to each other anyway and benefit other areas too.
Andrew: What about things like, for instance, some pregabalin, gabapentin, fraught with side effects? Not just that, but also titration issues. You've got to find the personalised dose. With regards to oral GABA, do you find that you've really got to play around with the dose that suits the patient? Or do you have a standard dose that tends to work for most people?
Elizma: The types of GABA, yeah. I usually find that most people will respond to maybe 200 milligrams of GABA if we're talking about the capsules. There are those occasions, especially when people have been addicted to benzodiazepines or are using benzodiazepines. You know, those receptors are so desensitised that you only need really large amounts of GABA in those people to work.
So, yeah. You sometimes have to adjust the dose, but it's always good to start low and then just work your way up and see how they go with it. When you use a more absorbable forms, like liposomal forms, then you can get away with a lot less. So, it'll depend on the delivery mechanism on I guess, how much you would want to use.
But I don't necessarily believe in more is better. It's always about the minimum dose that gives you the maximum benefit. So that's the way that I like to work.
Andrew: Yeah. I totally agree with you. I'm glad you say that because I really think it becomes this bang for buck question. You've really got to think, "Well, how much am I getting here? And how much is it costing the patient?
Elizma: Absolutely. And like I said, if you just have to give them GABA, GABA, GABA or dopamine all the time, then you need to look at it from a different perspective. You need to think, "Well, maybe the receptors are not working. So, am I doing a service to this person just pushing more substrate in and it's not actually binding to the receptors."
You know, it's the same as insulin resistance. If someone is insulin resistant, do you just want to give him more insulin or do you want to fix the insulin resistance? It's the same with dopamine and all of these other neurotransmitters. You want to fix the resistance. If they are not responding appropriately. So, it's not always about just driving more serotonin, dopamine or GABA into the body.
Andrew: I've long had a concern with bioidentical progesterone in that it is a band-aid. It's okay to use a band-aid if you've got a cut that's bleeding. You know, it's a short-term fix. But it's not going to really stop the issue. What do you advocate with regards to the hormonal treatment of dopaminergic or addiction issues?
Elizma: Well, the short-term would be to work on the neurotransmitters themselves. So, whether I'm using Rhodiola or GABA or what have you, it's trying to get that neurological effect quickly in so they can start to feel a little bit better.
But you're absolutely right. They should still not just be the focus because a lot of this is driven by inflammation. So you get increased cytokines and chemokines that creates inflammation in the brain, which then over activates this dopamine system. And you've got to be really careful with things like progesterone as well, Andrew, because if you give someone progesterone that has a lot of inflammation, oxidative stress and gut dysbiosis going on, then progesterone can actually become pro-inflammatory.
So, it's not always a great way to go even if they may need it. So, I would start looking for where is the inflammatory source coming from? Do they have gut dysbiosis? And I mean, so many people have gut dysbiosis. Do they maybe have viral infections or other infections or toxin overload? Or are they overtraining that might also be creating too much stress. Or is their diet bad? Because even inflammation can come from a bad diet. Too much sugars… and that's where it becomes tricky because a lot of that is driven by the addictive behaviour.
So, sometimes it's about making dietary changes. Sometimes it's about treating gut dysbiosis or infections. And I would really treat the root cause separately depending on what is it for that person.
But that is exactly what you should be doing is looking for the root cause. Just trying to patch it up with neurotransmitters and hormones is also not the long-term solution.
Andrew: Of course, you mentioned the granddaddy of treatment paradigms I think, and that's inflammation. And it just comes up time and time again.
As an intervention, do you tend to use these relaxing herbs, magnesium, maybe a little bit of zinc? To look at the underlying, let's say a more gentle, conceptual way of reducing inflammation. Or do you tend to use anti-inflammatories? Like curcumin is the poster child, but you've also got other things like Boswellia and things like that.
Elizma: I do use turmeric probably not as much as other practitioners. I guess I like to use the minerals as well, such as magnesium and things like that. Just sort of quiet down those MMDA receptors.
So, I like to focus on the brain inflammation from that perspective. But probably one of the...I would absolutely look at the dietary aspect. And I know the diet can sometimes be really hard for people, but just putting them on a Mediterranean style diet and start reducing their sugars and starting reducing that inflammation. Because I find even by doing things like turmeric it has very limited effect if there's still something majorly in their lifestyle that is driving that inflammation.
So, I may do like bits of everything. I'll add in some minerals, I'll add in things like the turmeric or Boswellia or herbs like that. And then absolutely make sure that there isn't anything in the diet that may be really affecting them. And I'm not necessarily saying that an extreme diet. But if there's something that really just stands out as like, "This is really not good." Then we need to work on that.
And let's say alcohol, let's say they’re drinking alcohol because, and that's causing a lot of inflammation. Then I may sort of say, "Well, let's do the GABA to try and reduce those alcohol cravings." So, we are not producing all of this inflammation.
So, it's just working it backwards and saying, "What is the biggest trigger of their inflammation? And seeing how best we can remedy that until we can dig deeper and deeper and get other things fixed along the way as well.
Andrew: What about co-treating within the medical paradigm?
Elizma: Well, yeah. You would absolutely never want to take anyone off any medications that was prescribed to them. And there's a lot of different ways that the medical paradigm works, as flawed as it is, in my opinion. There's a lot of drugs can be used and we can use a lot of our nutraceuticals along with these treatments without any effects.
I mean, if you look at what is the triggers for relapse, it's things like stress and depression, anger, anxiety, and cravings. And we can work on all those levels from a nutritional perspective. Now, you can use chromium for cravings. You can use things like GABA or kava for anxiety. You can work very well along these lines of addiction drugs, or drugs used in addiction, without compromising the effectiveness of the drugs, but maybe reducing the relapse or the risk of relapse when they are on these drugs.
I mean, the problem with the drugs, a lot of the drugs like the benzodiazepines that's used in alcohol addiction is that they can become addictive themselves. So, there's ...which is why it's not, in my opinion, a very good long-term solution. Apart from the fact that the relapse rates are so high.
So, I think using nutraceuticals in conjunction, it's a fantastic way to reduce that risk of relapse. And, you know, so that they can eventually come off the drugs and then maybe continue with some of the treatment strategies and keep themself free of these addictions for hopefully as long as they live.
Andrew: Where can practitioners find out more? What, in your opinion, are the best resources to go to?
Elizma: Well, there’s… I really love the research that's done by Dr Kenneth Blum. So, he's done some remarkable research and like I said, they're still in the process of doing research and they've got the substance… he developed a substance called KB22O which is also known as "synaptogenics or synaptamine." That they are trialing a lot of rehab clinics. And when I was looking at the results that they were getting with it in terms of cocaine addiction, heroin addiction, alcohol addiction, and how much it reduced relapse, it was just phenomenal. It was almost looking at it and you thought this cannot be true that something can be this effective.
Elizma: And these are all done through nutritional interventions. So, if you Google, I don't have a website. But if you Google him and his work, is there's a lot of research papers on that. Fascinating research on the whole dopaminergic system. So, that's probably one of the big sources that I would go to for information.
Andrew: Brilliant. So, we'll put that up on the FX Medicine website for our listeners. So, go to fxmedicine.com.au. Log in if you need to and you can find out more about all of the podcasts, but certainly about this one.
Elizma, thank you so much for taking us through that. That was really enlightening. I actually really admire the way that you say I'm not a specialist. I'm a generalist and there’s a reason for it.
But I do like the way that you connect the dots. You dive deeper into symptomatology and don't just think about attacking something on a surface level, but looking at the real reasons for the causation of it. Thank you very much.
Elizma: Thank you, Andrew.
Andrew: This is FX Medicine, I’m Andrew Whitfield-Cook.
|Dr Kenneth Blum|