SweetSue's Class Notes

[SweetSue]

From pages 144-145 of Uwe Blesching’s Cannabis Health Index:

“In 2007, a team from San Francisco examined cannabinoids in the context of cases involving a rapid spread of aggressive breast-cancer cells. To date, oncologists have a very limited set of options, each with its own toxic or adverse effects. In this experiment, scientists wrote about a key finding: ‘Here, we report that Cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate gene (Id-1) expression in aggressive cancer cells. [...]In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.’”

It’s been 12 years. I wonder what new developments have come along. I know Mara is strong on this therapeutic approach, because they’ve seen results.

More....

“Perhaps the most exciting research comes from Spain, where scientists discovered for the first time that cannabinoids therapeutics influence a genetic component involved in breast cancer progression. The authors wrote: ‘In summary, this is the first report showing not only that cannabinoids regulate a protein called transcription factor jun-D, which in humans is encoded in a JUND gene but, more generally, that Jim-D activation reduces the proliferation of cancer cells, which points to a new target to inhibit breast cancer progression.”

Also, this:

Moments of reflection for the cancer patient

• SweetSue
• Apr 4, 2019

From Uwe Blesching’s Cannabis Health Index

And this:

on my wish list

• SweetSue
• Apr 4, 2019
• 1

 

[SweetSue]

“As many patients have discovered, whenever we engage in the process of exploring and learning about evidence-based medicine and include a mind-body approach, we are empowered to make more informed decisions. Better decisions mean we have acces to more options and possibilities for regaining our health and fully healing.” - Uwe Blesching

Couldn’t have said it better myself. In my head it’s as simple as “You were evolved to heal. The more joyful you can become, the greater your chances of reaching homeostasis.” It really is about mind body. Any thought to the contrary ignores the total picture. Single-molecule medicine has perverted the healing stream. Sometimes it feels like we may be at the end of that maddening run of decades, and then they introduce yet another newer molecule and the game starts all over again.

 

[SweetSue]

“Equipped with evidence-based research at your fingertips, the task of making more informed decisions about medical cannabis becomes practical and doable.” -Uwe Blesching

This is exactly what we do here all day every day.

 

[SweetSue]

Coffee and health

“In summary
An increasing incidence of liver disease across Europe, associated in some cases with increases in metabolic syndrome, type 2 diabetes and obesity, is concerning, despite the fact that it is likely that diagnosed cases of liver disease represent only a small proportion of those with the condition. Physicians and patient associations are striving to improve diagnosis and subsequent treatment of liver conditions, as well as providing meaningful preventative advice to stem the increasing incidence. Research consistently suggests
that moderate coffee drinking (defined as 3–5 cups per day by EFSA) is associated with a reduced risk of liver disease.”

 

[Jdeck]

Oh, @SweetSue where have you been all my life? I’m along for the education your providing. Thank you

 

[SweetSue]

Oh, @SweetSue where have you been all my life? I’m along for the education your providing. Thank you

I’ve been right here for the past three + year’s Jdeck. Glad to meet you. It’s always a good day when another cannabis warrior steps up to learn more of the wonder of the ECS and how we can help support it with cannabis.

Am I right in assuming you grow cannabis on your deck?

Oh... and is there anything particular you were hoping to learn?

 

[Jdeck]

I’ve been right here for the past three + year’s Jdeck. Glad to meet you. It’s always a good day when another cannabis warrior steps up to learn more of the wonder of the ECS and how we can help support it with cannabis.

Am I right in assuming you grow cannabis on your deck?

Oh... and is there anything particular you were hoping to learn?

This is the first time I seen this thread. I’m a sponge, just soaking it all in. I am growing inside, I have a ex walk-in closet set up. I’ll certainly let you know of any questions after I get caught up. Thank you for the welcome.

 

[SweetSue]

This is the first time I seen this thread. I’m a sponge, just soaking it all in. I am growing inside, I have a ex walk-in closet set up. I’ll certainly let you know of any questions after I get caught up. Thank you for the welcome.

This is really my dumping ground for research material I use to build threads and answer member questions. The Cannabis Oil Study Hall is another massive info dump you might enjoy wandering through.

I have a wealth of threads running, enough that I’ve organized them myself in SweetSue’s Threads (see the signature line).

Have fun exploring.

 

[SweetSue]

Not the find I thought it was. This was dated Feb 8, 2019. They’re stepping up the propaganda game.

Ooooo.... great find.

I’ll be updating this as I go along. I got ahead of myself posting it.

At 7:35 she talks about the adaptability of the ECS. It learns from stress. A repeated stress will engender a faster response from the ECS.

Soooo freakin’ cool.

8:40 - the ECS actively works to prevent the formation of emotionally aversive memories. They prevent the consolidation and retrieval of emotionally aversive memories.

9:41 - They have questions about the safety of CBD.

What questions could they have about the pharmacological safety of CBD? I’m assuming pharmacological, since her field is researching the ECS.

A new mystery to follow up on.

10:14 - THC activates an eCBR and either
* mimics the ECS or
* disrupts the ECS

This is the first time I’ve heard it put like this. Not sure where this is going.

12:16 - “When THC is on board the ECS downregulates.”

How can this be true across the board? In a healthy system, already in tonal balance, yes, I can see this. In a system overwhelmed by THC, as in dabbing, yes, I understand that. But a system in distress? This seems counterintuitive.

12:30 - With THC present the system creates fewer eCBs and pulls receptors offline.

Part of what we’ve been told about CBD is that it’ll encourage a buildup of eCBs because it’ll block anandamide uptake.

Something’s not adding up.

13:00 In some people using cannabis to destress will instead become anxious.

T-E-R-P-E-N-E-S!

13:26 - Using cannabis to destress robs your ECS of the chance to improve your body’s ability to cope with stress.

Let me think this over. It doesn’t feel kosher at all. Bliss robs you of the ability to cope with stress the next time?

13:38 - She actually says that you use cannabis so you won’t do something else like exercise to help you better cope with stress. She actually said that cannabis use means you won’t explore other ways to support your ECS.

I thought, “Baby, you’ve never watched me get buzzed and do Callanetics.”

13:55 - We found our way to cannabis dependence. *sigh*

The worst consequence for most cannabis users is still having people find out. Social judgement is wicked deep on this planet. If cannabis didn’t cost so dearly and be so difficult to obtain it wouldn’t cause a lot of what they term “dependent behavior.” Wanting to stop and not being able to.... how much of the “wanting to stop” is social pressure? How much of the “not being able to stop” is really a reflection of overbearing oversight and control.

Yeah.... I’ve seen a lot of the dark side of cannabis “dependency.” Kids shipped off to military school. Parents wringing their hands thinking Jr. is a raving dope fiend when all he wanted was to focus on his studies. Rehab programs...... I have prejudices.

There’s a percentage of the population that’ll develop dependency of one thing or another. No denying that. Better cannabis than alcohol.

14:43 - This is interesting. Your ECS responds to sensory input and emotional response. THC, on the other hand, doesn’t respond to the environment and has multiple effects at once. Remember, the ECS creates on site, on demand.

15:12 - Again, the negative effects of THC being anxiety and psychosis. We’re gonna be years cleaning this pile up, eh?

THC “anxiety and psychosis” is controllable by dose, ratio, and scheduling. Terpenes have more to do with it than cannabinoids, IMO, unless you overdose, along with the reality that many people misinterpret their fear of letting go to paranoia.

16:15 - Following a litany of cautions about THC she allows that cannabis components, THC, and CBD in particular, may relieve some of the symptoms of some diseases.

16:28 - Her closing thoughts begin:

Cannabis may relieve symptoms acutely, but make disease worse in the long run. We don’t know.

16:46 - Our hope is in the future possibilities I’d pharmaceuticals that can upregulate or downregulate the ECS on demand and with more precision than cannabis does.

17:16 - “We need to assess the potential harms of recreational cannabis. “

 

[InTheShed]

Fascinating! Especially the part about THC downregulating the ECS.

 

[SweetSue]

Fascinating! Especially the part about THC downregulating the ECS.

Yeah. At 10:40 she veers off into crazy talk.

 

[SweetSue]

Unfreakin’believable!

• SweetSue
• Apr 4, 2019
• 3

She thinks it’s just a matter of probability that in the plant kingdom there’d be some plants that’s produce molecules that’d activate our receptors.

Ok... to be fair, I haven’t finished the video.

 

[SweetSue]

Fascinating! Especially the part about THC downregulating the ECS.

She made that into a bad thing.

 

[SweetSue]

Yeah. At 10:40 she veers off into crazy talk.

Propaganda frightens me. It works, and the opposition has learned a thing or two about packaging. A respected stage, pretty woman, pretty graphics. The audience misses the lies of omission and blatant misinformation and misinterpretation

Two steps forward, and they do their best to pull one step back.

 

[InTheShed]

I thought the graphics were kind of childish unless that was the audience she was targeting!

 

[Derbybud]

Same thought here.

 

[SweetSue]

Continuing on with Chapt 16 of Handbook of Cannabis

16.2.2 Distribution

THC concentrations decrease rapidly after smoking due to
*distribution into tissues,
*hepatic metabolism, and
* urinary and fecal excretion.

THC is highly lipophilic and rapidly taken up by highly perfused tissues, such as lung, heart, brain, and liver.

Highly perfused tissues are those with lots of fluid movement potential. Look at the ones that get the most action - lungs, heart, brain, liver. Highly vascularized, every one.

It is estimated that 2–22 mg THC is necessary to produce pharmacological effects in humans (Huestis 2005).

I wonder if this estimation has since been revised somewhere. We now have evidence of pharmacological effects in humans with micro doses of 1mg.

Assuming 10–25% smoked THC bioavailability, 0.2–4.4 mg THC is the required smoked dose, with about 1% or 2–44 micrograms THC in brain at peak concentration.

Whew! The variables! 2-44 micrograms at peak concentrations. Cannabis is an individual medicine to the extreme.

Equilibration between blood and tissue THC occurred approximately 6 h after an i.v. THC dose.

At approx. 6 hrs in there’s as much THC in the blood as in the tissues.

When 200 micrograms/kg intrajugular THC was administered to pigs, blood terminal half-life was 10.6 h and volume of distribution (Vd) 32 L/kg, much larger than found in humans (Brunet et al. 2006).

The authors observed that the pig had a higher percentage of body fat which may contribute to the larger Vd but believed the model yielded valuable data to assist in interpretation of human cannabinoid results.

THC concentrations 0.5 h after 200 micrograms/kg intrajugular THC were
* blood 24,
*kidney 272,
*heart 178
* lung 1888,
*muscle 55,
*spleen 34,
*fat 91,
*liver 155,
*brain 49,
*bile 0.4, and
*vitreous humor 1.2 micrograms/kg.

There’s a wee bit of difference between the pig biology and humans.

THC was eliminated fastest from liver and was unmeasureable after 6 h (<5 micrograms/kg).

THC concentrations decreased more slowly in brain than blood, but at 6 h were only 9% of those at 0.5 h.

If blood plasma is what we’re intent on, and it appears to be only a small part of what’s going on, then you want to dose every 4-6 hours, just as Cajun instructed us.

Fat had the highest THC retention, with detection beyond 24 h. 11-OH- THC was only found in liver, and

THCCOOH was less than or equal to 5 micrograms/kg in most tissues.

THCCOOH is the next to last step in the metabolism of cannabis, right before the molecules are prepared for elimination.


In a study of 25 frequent, long-term cannabis smokers

(12 males, 13 females),

investigators found that blood THC concentrations persisted for multiple days after cannabis discontinuation (Karschner et al. 2009).

Blood was collected during 7 days of monitored cannabis abstinence.

* Nine subjects (36%) had no measurable THC;
*16 had at least one positive THC of at least 0.25 micrograms/L, but not necessarily on the first day.
*On day 7, six participants still had detectable THC concentrations

- (mean ± SD, 0.3 ± 0.7 micrograms/L)​

and all 25 had measurable THCCOOH (p.301)

- (6.2 ± 8.8 micrograms/L).​

Five participants, all female, had THC-positive blood specimens over all 7 days. The authors re-emphasize that THC distributed to lipid stores in chronic cannabis users can be released into blood over many days.

THC metabolism to 11-OH-THC, THCCOOH, and phase II metabolites also contributes to THC reduction in blood.

When tritiated i.v. THC and 11-OH-THC pharmacodynamics and pharmacokinetics were compared,
* equal doses produced equal psychoactive effects,
* but the onset of effects and removal from the intravascular compartment was more rapid for 11-OH-THC (Huestis 2005).

The intravascular compartment is the lymph system.

The earlier results suggest that 11-OH-THC diffuses into human brain more readily than THC
* and that plasma protein binding of 11-OH-THC is lower than for THC.

Additional information about THC distribution from earlier studies include:
◆ Steady state Vd is about 3.4 L/kg.
◆ Less highly perfused tissues accumulate THC more slowly and release it over a longer period of time.
◆ THC stored in fat in chronic frequent cannabis smokers can be released into blood for days.

Because the degree of tolerance development following chronic frequent cannabis administration and the underlying mechanisms for tolerance were unclear, Gorelick et al. (2012) studied the development of tolerance following around-the- clock
* (every 3.5–6 h)
* 20 mg oral synthetic THC
*in 13 male daily cannabis smokers:
*40 mg day 1;
*100 mg days 2–4;
* and 120 mg days 5–7.

Systolic and diastolic blood pressure, heart rate, and symptoms of subjective intoxication (100 mm visual analogue scales) were assessed
* on the morning of day 1 (before oral THC),
* and on days 2, 4, and 6,

-every 30 min for 3 h after the first THC dose.​

​

Morning subjective intoxication ratings increased from days 1 to 2,

and then declined on days 4 and 6.

The morning THC dose increased intoxication ratings on day 2,

- but had less effect on days 4 and 6, a pattern consistent with tolerance.​

​

* THC lowered blood pressure and increased heart rate over 6 days.
* Plasma THC and 11-OH-THC increased significantly over the first 5 dosing days

- reaching mean Cmax of 30 and 15 micrograms/L on day 5.​

​

Six days of around-the-clock, oral THC produced tolerance to subjective intoxication, but not to cardiovascular effects.

THC rapidly crosses the placenta, although concentrations are lower in fetal blood and tissues than in maternal plasma and tissues (Huestis 2005).

How much lower? How many participants in the study?

THC metabolites, 11-OH-THC and THCCOOH, cross the placenta much less efficiently,
***and it is probable that THCCOOH does not pass from mother to fetus by placental transfer.

So not many test subject, one would assume. We build policy on these misguided studies.

THC in human umbilical cord blood is three to six times lower than in maternal blood, with greater transfer to the fetus early in pregnancy.

There it is. 3-6 times lower. Cool!

THC also concentrates into breast milk from maternal plasma due to its high lipophilicity.

Breast milk is filled with cannabinoids. It’s why infants bond when they nurse. It’s why they nurse to begin with. Cannabinoids signal the nursing response. Why, oh why are we so concerned about damaging little humans who have fewer receptors to activate? Babies can’t be hurt by cannabinoids anymore than adults.


To be continued.......

 

[SweetSue]

Same thought here.

That was such a strange thing to watch. It started out so well, and then went sideways just as you were getting into it. To suggest that it’s pure whimsical probability that cannabis alone has a wealth of components that interact with our cells, as though this kind of interaction is bound to suddenly pop up again with another plant.......

The way the opposition fights against science to make their erroneous points that cannabis is dangerous just makes me more creative in educating people in how safe it is.

 

[SweetSue]

An interesting comparison of the terpene profiles in 17 different chemovars. I’ll break it down later for better readability.

Source

Variations in Terpene Profiles of Different Strains of Cannabis sativa L
S. Casano, G. Grassi, V. Martini and M. Michelozzi (2011)
Variations in terpene profiles of different strains of Cannabis sativa L. Acta Horticulturae 925:115-121

[...]
The current study investigated the variability in terpene profiles of Cannabis strains and explored the utility of monoterpenes in the distinction between ‘mostly sativa’ and ‘mostly indica’ biotypes.

[...]

Table 1. Terpene profiles of different ‘mostly indica’ and ‘mostly sativa’ strains of Cannabis sativa L.
ND = not detected

Fig. 1. Comparison of terpene profiles in ‘mostly indica’ (black histograms) and in ‘mostly sativa’ (white histograms) strains of Cannabis sativa L. Break on Y-axis is 0.7-0.8. Numbers on X-axis refer to individual compounds: 1=α-pinene, 2=unk1, 3=unk2, 4=camphene, 5=β-pinene, 6=sabinene, 7=Δ-3-carene, 8=α-phellandrene, 9=β-myrcene, 10=α-terpinene, 11=limonene, 12=1.8 cineole, 13=γ-terpinene, 14=cis-β-ocimene, 15=trans-β-ocimene, 16=α-terpinolene, 17=unk3, 18=unk4, 19=β-caryophyllene, 20=unk5, 21=unk6, 22=unk7, 23=unk8, 24=unk9, 25=unk10, 26=unk11, 27=unk12 and 28=unk13.

Results and discussion
The relative content of terpenoids is strongly inherited while total yield per weight of tissue is more subjected to environmental factors. Expression of composition on a tissue basis (mg/g) is used for quality control and standardization of Cannabis cultivars, as well as for chemosystematic studies (Fischedick et al., 2010), but the relative content (%) of terpenoids is more often used for chemosystematic studies.

The average relative contents of dominant compounds detected in the aroma volatiles of all the strains were: β-myrcene (46.1±2.6%), α-pinene (14.0±1.5%), α-terpinolene (10.2±1.8%), limonene (7.3±1.3%), trans-β-ocimene (6.6±0.7%), β-pinene (6.1±0.4%), α-terpinene (3.6±1.0%), β-caryophyllene (1.2±0.2%), 1.8 cineole (1.1±0.2%), α-phellandrene (0.7±0.1%) and Δ-3-carene (0.6±0.1%). The average relative contents of camphene, unk1, cis-β-ocimene, unk5, unk8, unk7, unk13, sabinene, γ-terpinene, unk3, unk4, unk6, unk10, unk2, unk9, unk11 and unk12 were lower than 0.5%.

Results of Kruskal-Wallis ANOVA between different strains (d.f.=15, N=99) showed significant changes in relative contents of all the compounds: α-pinene (X2=71.6, P<0.001), unk1 (X2=71.5, P<0.001), unk2 (X2=43.6, P<0.001), camphene (X2=67.2, P<0.001), β-pinene (X2=53.2, P<0.001), sabinene (X2=72.5, P<0.001), Δ-3-carene (X2=69.4, P<0.001), α-phellandrene (X2=59.6, P<0.001), β-myrcene (X2=47.7, P<0.001), α-terpinene (X2=36.3, P<0.01), limonene (X2=77.1, P<0.001), 1.8 cineole (X2=67.5, P<0.001), γ-terpinene (X2=30.9, P<0.01), cis-β-ocimene (X2=79.5, P<0.001), trans-β- ocimene (X2=82.1, P<0.001), α-terpinolene (X2=78.7, P<0.001), unk3 (X2=37.6, P<0.001), unk4 (X2=33.7, P<0.01), β-caryophyllene (X2=55.7, P<0.001), unk5 (X2=65.6, P<0.001), unk6 (X2=74.4, P<0.001), unk7 (X2=50.1, P<0.001), unk8 (X2=64.7, P<0.001), unk9 (X2=63.2, P<0.001), unk10 (X2=61.1, P<0.001), unk11 (X2=80.1, P<0.001), unk12 (X2=61.8, P<0.001) and unk13 (X2=52.8, P<0.001).

β-myrcene was detected in high % in all the strains, with strain 17 having the highest relative content (80.1±7.3%) and strain 8 having the lowest relative content (16.1±3.4%) (Table 1). β-myrcene was the dominant terpene in almost all the strains, with the exceptions of strains 6, 7, 8 and 12. α-terpinolene was detected in high % in some ‘mostly sativa’ strains (7, 8, 9, 10 and 12), with strains 7 and 8 having α-terpinolene as the dominant terpene (respectively 41.8±7.2% and 37.3±3.5%), while it was not detected or it was detected in traces in ‘mostly indica’ strains and in some ‘mostly sativa’ strains (5, 6 and 11). α-pinene and β-pinene were detected in all the strains and their relative contents were commonly lower than 10%. α-pinene was detected in higher relative contents (up to 10%) in some strains (3, 6, 8, 11, 12, 14, 15 and 16), with strains 6 and 12 having α- pinene as the dominant terpene (respectively 46.3±5.7% and 24.2±15.6%). β-pinene was detected in higher relative contents (up to 10%) in strains 3 (12.6±1.6%) and 6 (13.2±0.8%). Limonene was detected in low % or traces in some ‘mostly indica’ strains (3, 14, 15 and 16) and in ‘mostly sativa’ strains, while it was detected in much higher % (up to 10%) in some ‘mostly indica’ strains (2, 4, 13 and 17), with these strains having limonene as second most abundant terpenoid. Trans-β-ocimene was not detected or it was detected in low % in one ‘mostly sativa’ strains (6) and in ‘mostly indica’ strains, while in some ‘mostly sativa’ strains (5, 7, 8, 9, 10, 11 and 12) it was detected in much higher % (up to 5%), with strains 5 and 11 having trans-β-ocimene as second most abundant terpenoid (respectively 18.7±1.9% and 16.8±2.2%). α-terpinene was detected in low % or traces in almost all the strains, with strain 4 having a much higher relative content (18.0±8.0%). The sesquiterpene β-caryophyllene was detected in all the strains and its relative content was commonly lower than 2%, with some strains (2, 9, 13 and 17) having relative contents up to 2%. 1.8 cineole was detected in low % (up to 2%) in some ‘mostly sativa’ strains (7, 8, 9, 10 and 12), while it was detected in lower % or traces in ‘mostly indica’ strains and in some ‘mostly sativa’ strains (5, 6 and 11). Δ-3-carene and α-phellandrene were detected in low % (up to 1%) in some ‘mostly sativa’ strains (7, 8, 9, 10 and 12), while they were not detected in ‘mostly indica’ strains and in some ‘mostly sativa’ strains (5, 6 and 11).

Mann-Whitney U test between ‘mostly sativa’ strains and ‘mostly indica’ strains (d.f.=1, N=99) showed significant changes in relative contents of several compounds except for α-pinene, unk2, β-pinene, α-terpinene, γ-terpinene, β-caryophyllene, unk7, unk12 and unk13 (Fig. 1). Relative contents of camphene (X2=22.7, P<0.001), β-myrcene (X2=23.1, P<0.001), limonene (X2=27.8, P<0.001), unk3 (X2=15.4, P<0.001), unk6 (X2=29.9, P<0.001) and unk11 (X2=42.3, P<0.001) were significantly higher in ‘mostly indica’ strains than in ‘mostly sativa’ strains (Fig. 1). Plants derived from ‘mostly sativa’ strains showed significantly higher relative proportions of unk1 (X2=33.4, P<0.001), sabinene (X2=24.9, P<0.001), Δ-3-carene (X2=39.6, P<0.001), α-phellandrene (X2=31.97, P<0.001), 1.8 cineole (X2=19.2, P<0.001), cis-β-ocimene (X2=48.6, P<0.001), trans-β- ocimene (X2=52.6, P<0.001), α-terpinolene (X2=13.2, P<0.001), unk4 (X2=15.3, P<0.001), unk5 (X2=29.6, P<0.001), unk8 (X2=24.3, P<0.001), unk9 (X2=7.5, P<0.01) and unk10 (X2=9.5, P<0.01) than plants derived from ‘mostly indica’ strains (Fig. 1).

Although Hillig (2004) stated that differences on terpenoids in Cannabis are of limited use for taxonomic discrimination at the species level, with sesquiterpenes generally more useful than monoterpenes, we found that several monoterpenes markers can be powerful tools for discerning between ‘mostly sativa’ and ‘mostly indica’ biotypes (Table 1 and Fig. 1). Our results are also supported by results recently obtained by Fischedick et al. (2010) showing that monoterpenes are able to distinguish cultivars with similar sesquiterpenes and cannabinoids levels.

Conclusions
The main differences between terpene profiles of the evaluated strains belonging to the two principal biotypes were that ‘mostly indica’ strains were characterized by dominancy of β-myrcene, present in high relative contents, with limonene or α-pinene as second most abundant terpenoid, while ‘mostly sativa’ strains were characterized by more complex terpene profiles, with some strains having α-terpinolene or α-pinene as dominant terpenoid, and some strains having β-myrcene as dominant terpenoid with α-terpinolene or trans-β-ocimene as second most abundant terpenoid.

This wide variability in terpene composition can provide a potential tool for the characterization of Cannabis biotypes, and warrant further researches in order to evaluate the drug’s medical value and, at the same time, to select less susceptible chemotypes to the attack of herbivores and diseases. More detailed studies on the variability in monoterpenes and sesquiterpenes are needed. Breeding for specific terpenoids in plants is a fascinating research topic; in fact, the various biological activities of these compounds make the analysis of terpenoids a valuable tool for improving a considerable number of traits in pharmaceutical and industrial cultivars of Cannabis.

Terpenoids analysis, combined with cannabinoids and flavonoids analyses, are essential for the metabolic fingerprinting of pharmaceutical cultivars. Pharmaceutical cultivars of the two principal biotypes may exhibit distinctive medicinal properties due to significant differences in relative contents of terpenoids, thus the synergy between the various secondary metabolites must be investigated in deeper details in the future in order to better elucidate the phytocomplex of Cannabis and to allow selection of chemotypes with specific medical effects.

 

[SweetSue]

Study joy

• SweetSue
• Apr 7, 2019

Study joy

• SweetSue
• Apr 7, 2019

Sometimes I wonder how I keep up with myself. This is only a small part of what I’m playing with. This is only the study side. This week.